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KAPLAN - Immunology > Kaplan - Immunology > Flashcards

Kaplan - Immunology Flashcards

1
Q

What is the body’s first line of defense and what are its defensive barriers?

A

Innate Immunity

  1. Anatomic/Physical (skin, mucous membranes, flora)
  2. Physiologic (temperature, pH, antimicrobials, cytokines)
  3. Complement
  4. Cellular: Phagocytes and granulocytes
  5. Inflammation
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2
Q

Which immunity has no memory, limited specificity, present intrinsically?

A

Innate immunity

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3
Q

What makes up the adaptive immunity?

A

T lymphocytes
B lymphocytes
Their effector cells

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4
Q

What is immunologic memory?

A

Are capable of distinguishing self from non self

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5
Q

What is the difference between Sensitivity and Specificity?

A

Sensitivity (also called the true positive rate) measures the proportion of positives that are correctly identified as such (e.g. the percentage of sick people who are correctly identified as having the condition).

Specificity (also called the true negative rate) measures the proportion of negatives that are correctly identified as such (e.g. the percentage of healthy people who are correctly identified as not having the condition).

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6
Q

What is Sensitivity?

A

Sensitivity (also called the true positive rate) measures the proportion of positives that are correctly identified as such (e.g. the percentage of sick people who are correctly identified as having the condition).

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7
Q

What is Specificity?

A

Specificity (also called the true negative rate) measures the proportion of negatives that are correctly identified as such (e.g. the percentage of healthy people who are correctly identified as not having the condition).

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8
Q

What is self-limitation and why do we need it?

A

allows the system to return to a basal resting state after a challenge to conserve energy and resources and to avoid uncontrolled cell proliferation resulting in leukemia or lymphoma.

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9
Q

Which type of immunity has the ability of self-reactivity?

A

Neither, idiot

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10
Q

What are the anatomic and physiologic barriers of the two types of immunity?

A

Innate: skin, mucosa, normal flora, temperature, pH, antimicrobials, and cytokines

Adaptive: lymph nodes, spleen, mucosal-associated lymphoid tissues

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11
Q

What are the cell types of the two types of immunity?

A

Innate: Phagocytes, granulocytes, and natural killer

Adaptive: B lymphocytes and T lymphocytes

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12
Q

What are the blood proteins of the two types of immunity?

A

Innate: compliment

Adaptive: Antibodies

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13
Q

How long does it take the adaptive immune response to begin clearance of the infection through the action of effector cells and antibodies?

AKA when does the adaptive immune response begin?

A

1 - 2 weeks after primary infection for the adaptive immune response to begin clearance of the infection

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14
Q

What kind of mechanism does the innate and adaptive immune system use to work together?

A

Positive feedback mechanism

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15
Q

What is ontogeny/ontogenesis?

A

the development of an individual organism or anatomical or behavioral feature from the earliest stage to maturity.

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16
Q

What is hematopoiesis?

A

Production, development, differentiation and maturation of the blood cells (erythrocytes, megakaryocytes, and leukocytes) from multipotent stem cells.

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17
Q

Which cells are considered blood cells?

A

Erythrocytes
megakaryocytes
leukocytes

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18
Q

From which cell is hematopoeisis derived from?

A

multipotent stem cells

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19
Q

site of hematopoiesis during embryogenesis and early fetal development?

A

yolk sac

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20
Q

site of hematopoiesis during organogenesis?

A

liver and spleen

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21
Q

site of hematopoiesis during adulthood?

A

bone marrow

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22
Q

What kind of division do multipotent stem cells go through in the bone marrow?

A

asymmetric division

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23
Q

What do the two daughter cells from asymmetric division from multipotent stem cells from bone marrow do?

A
  1. self renewal

2. gives rise to either a common lymphoid progenitor cell or a common myeloid progenitor cell (potency)

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24
Q

Common Lymphoid progenitor cells give rise to:

A

B lymphocytes, T lymphocytes, and Natural Killer cells

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25
Q

Common Myeloid progenitor cells give rise to:

A

erythrocytes, megakaryocytes/thrombocytes, mast cells, eosinophils, basophils, neutrophils, monocytes/macrophages, and dendritic cells

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26
Q

Are natural killers innate or adaptive immunity?

A

NK are from lymphoid lineage but participate in innate immunity.

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27
Q

What differences of cell lineage does the B and T lymphocytes have?

A

B lymphocytes remain within the BONE MARROW to complete their development.

T lymphocytes leave the bone marrow and undergo development within the THYMUS.

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28
Q

What is the Third lymphocyte?

A

Natural Killers; they recognize tumor and virally infected cells through non specific binding.

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29
Q

What is the most abundant circulating blood cell?

A

Neutrophril or polymorphonuclear (PMN) cell

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30
Q

Neutrophril or polymorphonuclear (PMN) cell function?

A

Phagocytic activity aimed at killing extracellular pathogens.

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31
Q

lymphocyte cell function?

A

No function until activated in secondary

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32
Q

plasma cell function?

A

Terminally differentiated B lymphocyte that secretes antibodies.

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33
Q

Natural Killer Cell function?

A

Kills virally infected cells and tumor cells.

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34
Q

Monocyte function?

A

Precursor of tissue macrophage

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35
Q

Macrophage function?

A

Phagocyte
Professional Antigen presenting cell
T-cell activator

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36
Q

Dendritic cell function?

A

Phagocyte
Professional Antigen presenting cell
T-cell activator

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37
Q

Eosinophil function?

A

Elimination of large extracellular parasites

Type 1 hyperxdennsitivity

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38
Q

Mast cell function?

A

Elimination of large extracellular parasites

Type 1 hypersensitivity

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39
Q

Basophil function?

A

Elimination of large extracellular parasites

Type 1 hypersensitivity

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40
Q

Physical description:

Granulocyte with a segmented lobular nuclei (3-5 lobes) and small pink cytoplasmic granules

A

Neutrophil or Polymorphonuclear (PMN) cell

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41
Q

Physical description:

Large, dark staining nucleus with a thin rim of cytoplasm.

A

Lymphocyte

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42
Q

Surface markers:

B lymphocytes:

A

CD19, 20, 21

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43
Q

Surface markers:

T lymphocytes:

A

CD3

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44
Q

Surface markers:

Helper T cells:

A

CD4

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45
Q

Surface markers:

CTLS:

A

CD8

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46
Q

Physical description:

Small eccentric nucleus, intensely staining Golgi Aparatus.

A

Plasma Cell

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47
Q

Physical description:

Lymphocyte with large cytoplasmic granules

A

Natural Killer Cell

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48
Q

Surface markers:

Natural Killer Cells

A

CD 16, 56

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49
Q

Physical description:

Agranulocyte with a bean or kidney shaped nucleus.

A

Monocyte

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50
Q

Physical description:

Agranulocyte with a ruffled cytoplasmic membrane and cytoplasmic vacuoles and vesicles.

A

Macrophage

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51
Q

Physical description:

Agranulocyte with thin, stellate cytoplasmic projections

A

Dendritic cell

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52
Q

Physical description:

Granulocyte with bilobed nucleus and large pink cytoplasmic granules

A

eosinophil

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53
Q

Physical description:

Granulocyte with small nucleus and large blue cytoplasmic granule

A

Mast Cell

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54
Q

Physical description:

Granulocyte with bilobed nucleus and large blue cytoplasmic granules

A

Basophil

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55
Q

What is the most common leukocyte evaluated in a WBC differential of an adult?

A

Nuetophils (PMNs) 50-70%

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56
Q

What are the 2 isotopes of antibody or immunoglobulin expressed on surface membrane of mature, naive B lymphocytes?

A

IgM

IgD

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57
Q

What is expressed on surface membrane of mature, naive T lymphocytes?

A

T-Cell receptor (TCR)

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58
Q

Heavy chain and Light chain are the membrane bound immunoglobulin of which type of lymphocyte?

A

B lymphocyte

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59
Q

What holds together a heavy and light chains?

A

disulfide bond which makes the two halves resemble a “Y” shape

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60
Q

What is the “Y” shape of the B lymphocyte called?

A

hinge region

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61
Q

Which antigen receptor has:

  • membrane bound immunoglobulin
  • is a 4 chain glycoprotein molecule
  • two halves held together by disulfide bond
  • shape resembling “Y”
  • hinge region
  • flexible
A

Antigen receptor of the B lymphocyte

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62
Q

Which antigen receptor has:

  • alpha chain
  • beta chain
  • antigenic peptide complexed to an MHC molecule
  • No hinge region –> rigid
A

Antigen receptor of the T lymphocyte

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63
Q

the membrane receptors of B lymphocytes are designed to bind ______

A

unprocessed antigens of almost any chemical composition ie. polysaccharide, proteins, lipids,

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64
Q

the membrane receptors of TCR are designed to bind ______

A

peptides complexed to MHC

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65
Q

What is the signal transduction complex?

A

When a lymphocyte binds to an antigen complementary to its idiotype, a cascade of messages transferred through its signal transduction complex will culminate in intracytoplasmic phosphorylation events leading to activation of the cell.

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66
Q

CD21 is the receptor to what?

A

EBV

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67
Q

CD81 is the receptor to what?

A

Hepatitits C and Plasmodium vivax

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68
Q

How do B lymphocyte progenitors produce heavy chain variable domains?

A

B lymphocyte progenitors select randomly and in the absence of stimulating antigen to recombine 3 gene segments designated variable (V), diversity (D) and joining (J) out of hundreds of gremlin encoded possibilities to produce unique sequences of amino acids in the variable domains (VDJ recombination)

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69
Q

What is an idiotype?

A

antigen specificity

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70
Q

What is the point in VDJ rearrangements in DNA?

A

to produce the diversity of heavy chain variable domains

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71
Q

The enzymes responsible for gene rearrangements in lymphocyte development are called?

A

RAG1 and RAG2

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72
Q

The B-lymphocyte progenitor performs random rearrangements of 2 types of gene segments to encode the variable domain amino acids of the light chain. which are the two gene segments?

A

V and J

VJ rearrangements in DNA produce the diversity of light chain variable domains.

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73
Q

What is the function of the enzyme terminal deoxyribonucleotidyl transferase (Tdt)?

A

While heavy chain gene segments are undergoing recombination the enzyme Tdt randomly inserts bases (without a template on the complementary strand) at the junctions of V, D, J segments (n-nucleotide addition)

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74
Q

What is the function of N-nucleotide addiotn?

A

The random addition of the nucleotide generates junctional diversity.

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75
Q

What is apoptosis?

A

Programmed cell death

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76
Q

What is the function of allelic exclusion?

A

The process that ensures that B and T lymphocytes synthesize only ONE specific antigen receptor per cell.

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77
Q

Which cells are capable of N-nucleotide addition?

A 
B cells (only heavy chain)
T cells (all chains)
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78
Q

Omenn Syndrome:

Genetics?

Molecular defect?

Symptoms?

A

Omenn Syndrome:

Genetics: Autosomal recessive

Molecular defect: Missense mutation in RAG genes. The RAG enzyme have only partial activity.

Symptoms:

  • Lack of B cells (below limits of detection).
  • Marked decrease in predominantly Th2
  • Characterized by early onset, failure to thrive, red rash (generalized), diarrhea, and severe immune deficiency.
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79
Q

Severe Combined Immunodeficiency (SCID):

Genetics?

Molecular defect?

Symptoms?

A

Genetics: Autosomal recessive

Molecular defect: Null mutations in RAG1 or RAG2 genes. No RAG enzyme activity.

Symptoms:

  • Total lack of B and T cells.
  • Total defects in humoral and cell mediated immunity.
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80
Q

What kind of lymphoid organ is the bone marrow?

A

Primary lymphoid organ.

As lymphoid progenitors develop in the bone marrow, they make random rearrangements of their germline DNA to produce the unique idiotypes of antigen-recognition molecules that they will use throughout their lives.

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81
Q

What is clonal deletion and clonal anergy?

A

clonal deletion: cells deleted in bone marrow

clonal anergy: cells inactivated in the periphery

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82
Q

Which are the only b lymphocytes released to the periphery and allowed to leave the bone marrow?

A

Selectively unresponsive (tolerant) to self antigens are allowed to leave the bone marrow.

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83
Q

What is the second primary lymphoid organ?

A

Thymus, the second primary lymphoid organ dedicated to maturation of T cells.

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84
Q

How is a pre thyme cell considered a double negative T lymphocyte?

A

If they do not express CD4 or CD8 on their surface

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85
Q

What is a double positive thymocyte?

A

T-cell receptors that coexpress the CD3 complex as well as the CD4 and CD8 co receptors

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86
Q

What is MHC, whats their function?

A

To avoid binding to normal self-antigens and cause autoimmunity, Major Histocompatibility complex exposed developing thymocytes to high level of unique group of membrane bound molecules.

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87
Q

Where are the MHC located at?

A

They are membrane bound molecules.

Are a collection of highly polymorphic genes on the short arm of chromosome 6 in the human.

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88
Q

What is another name for MHC gene products?

A

human leukocyte antigens (HLA)

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89
Q

Name the gene products of Class I MHC:

A

HLA-A, HLA-B, HLA-C

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90
Q

Name the gene products of Class I MHC:

A

HLA-DM, HLA-DP, HLA-DQ, HLA-DR

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91
Q

Where are class I molecules expressed on?

A

All nucleated cells in the body, as well as platelets.

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92
Q

In what kind of fashion are class I molecules expressed?

A

Codominant fashion, meaning that each cell expresses 2 A, 2 B, 2 C products (one from each parent).

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93
Q

Where are class II molecules expressed on and in what fashion?

A

Class II MHC molecules are expressed (also codominantly) on the professional antigen-presenting cells of the body (primarily the macrophages, B lymphocytes, and dendritic cells).

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94
Q

In terms of MHC, what are:

positive selection
failure of positive selection
negative selection

A

● Those that have TCRs capable of binding with low affinity will receive a positive selection signal to divide and establish clones that will eventually mature in the medulla.

● Those that fail to recognize self-MHC at all will not be encouraged to mature (failure of positive selection).

● Those that bind too strongly to self MHC molecules and self-peptide will be induced to undergo apoptosis (negative selection) because these cells would have the potential to cause autoimmune disease.

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95
Q

How do thymocytes decide to become CD4 or CD8?

A

Although double positive thymocytes co-express CD4 and CD8, the cells are direct- ed to express only CD8 if their TCR binds class I molecules, and only CD4 if their TCR binds class II molecules

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96
Q

Which cells become “helper” cells (Th cells) and which cells become Cytotoxic T lymphocytes (CTL)?

A

CD4+ cells that recognize class II MHC are destined to become “helper” T cells ( ), and CD8+ cells that recognize class I MHC are destined to become cytotoxic T lymphocytes (CTLs).

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97
Q

What are regulatory T cells (Tregs) and what is their function?

A

Tregs inhibit self-reactive Th1 cells in the periphery.

● Identified by their constitutive expression of CD25 on the surface and by the expression of the transcription factor FoxP3
● Secrete IL-10 and TGF-β which inhibit inflammation
● Shown to be critical in the prevention of autoimmunity

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98
Q

What is the primary job of a cytokine?

A

initiate an inflammatory response

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99
Q

What can a defensin found in a phagocyte do?

A

They can cause pores in bacteria and fungi.

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100
Q

Phagocytic cells are part of the first line of defense against invading pathogens. They recognize pathogens via shared molecules that are not expressed on host cells. They are responsible for controlling the infections and sometimes are even capable of eradicating them.

Name the most common phagocytic cells.

A

monocytes/macrophages, neutrophils and dendritic cells

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101
Q

What are the receptors of the innate immune System and what is it function?

A

Pattern recognition receptors (PRRs).

They recognize pathogen associated molecular patterns (PAMPs) or damage associated molecular patterns (DAMPSs)

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102
Q

The inflammasome is an important part of the innate immune system. It is expressed in myeloid cells as a signalling system for detection of pathogens and stressors. Activation of the inflammasome results in the production of _________ and ________, which are potent in inflammatory cytokines.

A

IL-1β and IL-18

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103
Q

Which myeloid cells are CD14 positive?

A

Monocyte, macrophage, Neutrophil, dendritic cells

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104
Q

Which innate immunity cells is this:

● Circulating phagocytes
● Short lived
● Rapid response, not prolonged defense

A

Neutrophils

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105
Q

Which innate immunity cells is this:

● Provide a prolonged defense
● Produce cytokines that initiate and regulate inflammation
● Phagocytose pathogens
● Clear dead tissue and initiate tissue repair

A

Monocytes/ macrophages

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106
Q

Whats the relationship of a Monocytes/ macrophages?

A

Monocytes circulate in the blood, become macrophages in the tissues

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107
Q

What are the two pathways for macrophage activation?

A

Classical M1:
Induced by innate immunity (TLRs, IFN-y)
Phagocytosis, initiate inflammatory response

Alternative M2:
Induced by IL-4, IL-13
Tissue repair and control of inflammation

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108
Q

Which innate immunity cells is this:

● Found in all tissues
● Antigen processing and presentation
● Two major functions: initiate inflammatory response and stimulate adaptive immune response

A

Dendritic Cells (DCs)

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109
Q

Which innate immunity cells is this:

● Skin, mucosa
● 2 pathways for activation: innate TLRs and antibody-dependent (IgE)

A

Mast cells

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110
Q

Which innate immunity cells is this:

● Blood, periphery
● Direct lysis of cells, secretion of IFN-γ

A

Natural Killer Cells (NK cells)

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111
Q

The complement system is a set of interacting proteins released into the blood after production in the liver. The components act together as zymogens, activating one another in cascade fashion after initiation from a variety of stimuli.

What are the 3 functions of the complement system?

A
  1. Recruitment of inflammatory cells and anaphylatoxins
  2. Opsonization of pathogens
  3. Killing of pathogens
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112
Q

What is Leukocyte adhesion deficiency (LAD) and what are its symptoms?

A

Rare autosomal recessive disease in which there is an absence of CD18 (the common B2 chain of a number of integral molecules).

A key element in the migration of leukocytes is integrin-mediated cell adhesion; patients suffer from an inability of their leukocytes to undergo adhesion dependent migration into sites of inflammation.

opmphalitis, abscess and pus do not occur, more susceptible to recurrent, chronic bacterial infections.

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113
Q

What is the first indication of Leukocyte adhesion deficiency (LAD)?

A

The first indication of this defect is often omphalitis, a swelling and reddening around the stalk of the umbilical cord.

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114
Q

How do you diagnose Leukocyte adhesion deficiency (LAD)?

A

Evaluating expression (or lack) of the B chain (CD18) f the intern by flow cytometry.

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115
Q

What are the five steps of phagocytosis?

A
  1. Extension of pseudopodia to engulf attached material
  2. Fusion of the pseudopodia to trap the material in a phagosome
  3. Fusion of the phagosome with a lysosome to create a phagolysosome
  4. Digestion
  5. Exocytosis of digested contents
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116
Q

What is pus?

A

Neutrophils release granule contents into extracellular milieu during phagocytosis and inflammation in which the neutrophils die, forming what is known as pus.

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117
Q

What is a respiratory burst and what are the two oxygen dependent mechanisms of intracellular digestion that are activated as a result of this process?

A

During phagocytosis, a metabolic process known as the respiratory burst activates a membrane-bound oxidase that generates oxygen metabolites, which are toxic to ingested microorganisms. Two oxygen-dependent mechanisms of intracellular digestion are activated as a result of this process.

● NADPH oxidase reduces oxygen to superoxide anion, which generates hydroxyl radicals and hydrogen peroxide, which are microbicidal.

● Myeloperoxidase in the lysosomes acts on hydrogen peroxide and chloride ions to produce hypochlorite (the active ingredient in household bleach), which is microbicidal.

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118
Q

What is hypochlorite?

A

the active ingredient in household bleach

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119
Q

What is Chronic granulomatous disease (CGD)?

A

an inherited de ciency in the production of one of several subunits of NADPH oxidase. This defect eliminates the phagocyte’s ability to produce many critical oxygen-dependent intracellular metabolites.

• If the patient is infected with a catalase-positive organism (e.g., Staphylococcus, Klebsiella, Serratia, Aspergillus), the myeloperoxidase system lacks its substrate (because these organisms destroy H2O2), and the patient is left with the oxygen- independent lysosomal mechanisms that prove inadequate to control rampant infections.

Thus, CGD patients suffer from chronic, recurrent infections with catalase-positive organisms.

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120
Q

What are some catalase positive organisms?

A

Staphylococcus, Klebsiella, Serratia, Aspergillus

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121
Q

How can you detect failures of phagocytic cells to generate oxygen radicals?

A

Nitroblue tetrazolium (NBT) reduction tests or neutrophil oxidative index (NOI; a flow cytometric assay).

The dihydrorhodamine test -a similar test using flow cytometry may be used.

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122
Q

How can you tell if the results of a nitro blue tetrazolium reduction are normal or abnormal?

A

Normal: formazan positive (purple-blue)
Abnormal: formazan negative (yellow)

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123
Q

The innate response to viruses is unique in that it is geared toward eliminating these intracellular pathogens. The 2 major mechanisms for dealing with viral infections are ________.

A

IFN-α/β

NK cells.

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124
Q

How do interferons work on viruses?

A

Act on target cells to inhibit viral replication, not the virus.
Are not virus-specific

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125
Q

What are the therapeutic uses of IF alpha?

A

has well-known antiviral activity and has been used in the treatment of hepatitis B and C infections.

Within cancer therapy, it has shown promise in treatment of hairy B-cell leukemia, chronic myelogenous leukemia, and Kaposi sarcoma.

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126
Q

What are the therapeutic uses of IF beta?

A

was the first drug shown to have a positive effect on young adults with multiple sclerosis. Patients treated with It enjoy longer periods of remission and reduced severity of relapses.

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127
Q

What are the therapeutic uses of IF y?

A

being used in the treatment of chronic granulomatous disease (CGD). This molecule is a potent inducer of macrophage activation and a promoter of inflammatory responses. Its application appears to significantly reverse the CGD patient’s inability to generate toxic oxygen metabolites inside phagocytic cells.

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128
Q

What increases the activity of NK?

A

NK activity is increased in the presence of interferons (IFNs) a and b and IL-12

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129
Q

NK cells employ 2 categories of receptor:

A

NK cells employ 2 categories of receptor: killer activating receptor (KAR) and killer inhibitory receptor (KIR).

If only KARs are engaged, the target cells will be killed. If both the KIRs and the KARs are ligated, the target cell lives. Therefore the inhibitory signals trump the activation signals.

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130
Q

What is NKG2D?

A

NKG2D is a major KAR expressed by NK cells.

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131
Q

What is an inflammasome?

A

Inflammasome: a signaling system for detection of pathogens and stressors which result in the production of IL-1β and Il-18; these cytokines play a major role in the inflammatory response

The signals which trigger inflammasome activation recognize both microbial products and material from dead and dying cells.

132
Q

What are interferons alpha and beta?

A

Interferons alpha and beta (IFNα and IFNβ) are proteins released from virally infected cells that afford anti-viral properties to neighboring cells.

133
Q

What do NK cells kill and what are their weapons?

A

NK cells kill tumor and virus-infected cells using granzymes and perforin

134
Q

What stimulates NK cells and what do they target?

A

NK cells are stimulated by IFN-α, IFN-β, and IL-12, and kill targets lacking MHC I.

135
Q

Name secondary lymphoid organs and their function?

A

Lymph nodes and spleen

The sites where naive mature lymphocytes will first be exposed to their specific antigens

136
Q

What is the function of the lymph nodes?

A

They are designed to initiate immune responses to tissue borne antigens.

137
Q

What is the spleen and its function.

A

The spleen is the secondary lymphoid organ that initiates immune responses to blood borne antigens.

138
Q

Whats an antigen?

A

a toxin or other foreign substance that induces an immune response in the body, especially the production of antibodies.

139
Q

Whats another name for perianteriolar lymphoid sheaths (PALS) and what is its function?

A

Periarteriolar lymphoid sheaths (or periarterial lymphatic sheaths, or PALS) are a portion of the white pulp of the spleen. They are populated largely by T cells and surround central arteries within the spleen; the PALS T-cells are presented with blood borne antigens via myeloid dendritic cells.

140
Q

What is the exogenous pathway of MHC loading?

A

Its to elicit the adaptive immune response to a primary antigenic challenge by processing of antigen for the presentation to naive T lymphocytes.

141
Q

What is the endogenous pathway of MHC loading?

A

The endogenous pathway of antigen processing handles threats to thee host which are intracellular. These might include viruses, altered/mutated genes (from tumors).

142
Q

How are intracellular proteins routinely targeted and how are they degraded?

A

Targeted by ubiquitin

Degraded in proteasomes

143
Q

What is the Tap complex?

A

Peptides from proteins in the endogenous pathway of MHC loading are transported through a peptide transporter known as TAP Complex (transported of antigen processing) and into ER where they have the opportunity to bind to freshly synthesized MHC class I molecules.

144
Q

How do proteasome inhibitors work in treatment in cancer?

A

Proteasome inhibitors induce apoptosis in tumor cells by interfering with the degradation of regulatory proteins.

Proteasome inhibitors will produce an accumulation of p53 as well as other regulatory proteins, and therefore eventual cell death via apoptosis.

145
Q

What is Bortezomib used for?

A

FDA approved proteasome inhibitors in clinical use.

Currently approved to treat multiple myeloma and mantle cell lymphoma (clinical trials fro leukemia)

146
Q

What is Carfilzomib used for?

A

FDA approved proteasome inhibitors in clinical use.

Currently approved to treat multiple myeloma (clinical trials for leukemia and lymphomas)

147
Q

What is cross Priming?

A

Dendritic cells may activate both CD4+ T cells and CD8+ T cells (cross priming) which is essential in the development of CTL’s and CD8+ memory cells.

148
Q

What is CTLA-4?

A

CTLA-4 is an important immunoregulatory molecule in the immune system. Expressed on both activated Th and Tregs, CTLA-4 is responsible for downregulating the immune response by competitive binding to B7-1 and B7-2 on APCs.`

149
Q

What is Abatacept used for?

A

Agonist of CTLA-4 regulation

Clinical use: Rheumatoid Arthritis

150
Q

What is Belatacept used for?

A

Agonist of CTLA-4 regulation

Clinical use: Renal transplants

151
Q

What is Ipilimumab used for?

A

Aagonist of CTLA-4 regulation

Clinical use: Melanoma and in clinical trials for several other types of cancer

152
Q

There are 3 major classes of helper T (Th) cell that arise from the same precursor, the naive Th lymphocyte (or Th0 cell): what are the 3 major classes?

A

Th1
Th2
Th17

153
Q

What gets the Th1/T-bet up and running?

A

Intracellular infections, IL-12

154
Q

IL-12 –> Th1/T-bet –> _____

A

IFN-y

155
Q

What gets the Th2/GATA3 up and running?

A

Parasitic infections

IL4

156
Q

IL-4 –> Th2/GATA3 –> _____

A 
IL-4
IL-5
IL-10
IL-13
TGF-B
157
Q

What gets the Th17/RORyT up and running?

A

Extracellular Bacterial and Fungal infections

IL-23, IL-6, TGF-B

158
Q

What is responsible for this:

Amplifies Th1 response
Inhibits Th2 response
Activates classic macrophage
Drives isotype switching to IgG

A

IFN-y

159
Q

IL-23, IL-6, TGF-B –> Th17/RORyT –> _____

A

IL-17, IL-22

160
Q

What causes Leprocy and what are the two different types?

A

Mycobacterium leprea

Tuberculoid leprosy
Lepromatous leprosy

161
Q

Which type of leprosy is this?

The patient has a strong Th1 response, which eradicates the intracellular pathogens by granuloma formation. There is some damage to skin and peripheral nerves, but the disease progresses slowly, if at all, and the patient survives.

A

tuberculoid leprosy

162
Q

Which type of leprosy is this?

The Th2 response is turned on, and because of reciprocal inhibition, the cell-mediated response is depressed. Patients develop antibodies to the pathogen that are not protective, and the mycobacteria multiply inside macrophages, sometimes reaching levels of 1010 per gram of tissue. Hypergammaglobulinemia may occur, and these cases frequently progress to disseminated and disfiguring infections.

A

Lepromatous leprosy

163
Q

What is a Thymus independent (TI) antigen?

A

Certain mature, naïve B lymphocytes are capable of being activated by macromolecules such as lipids, polysaccharides, and lipopolysaccharides without having to interact with helper T cells. These antigens are called thymus-independent (TI) antigens, and they directly stimulate B cells to proliferate and differentiate into plasma cells.

The response to TI antigens is generally weaker than the response to TD antigens, resulting primarily in the secretion of IgM antibodies and the absence of immunologic memory.

164
Q

What is a Thymus Dependent (TD) antigen?

A

Most antigens introduced in the body fall into the category of thymus-dependent (TD) antigens. Response to such molecules requires the direct contact of B cells with helper T cells and are in influenced by cytokines secreted by these cells. After the cross- linking of receptors on the B-cell surface with antigen, the material is endocytosed and processed via the exogenous pathway to generate an MHC class II: peptide complex, which is then inserted into the membrane of the professional APCs.

165
Q

Because binding antigen serves as the first signal for proliferation, over time clones of cells with higher receptor affinity will begin to predominate in the germinal center. This clonal selection results in the predominance of clones capable of producing anti- bodies with increasing affinity for the antigen, a process known as a ________.

A

affinity maturation

166
Q

During the activation of B lymphocytes by helper T cells, intense proliferation of the B cells results in the formation of germinal centers in the follicles of the secondary lymphoid tissues. These are clones of proliferating, antigen-specific cells. During the intense proliferative response of the B cell, random mutations in the coding of the variable domain region may occur. This is called __________ and creates single point mutations in the antibody idiotype. If these slightly altered idiotypes have increased affinity for the antigen, then the cell expressing them will be at a selective advantage in competing to bind antigen.

A

somatic hypermutation

167
Q

Which is the principal immunoglobulin of the primary immune response produced by a B cell with or without T-cell help when antigen is first encountered?

A

IgM

168
Q

Which cells are CD25+ and express the FoxP3 transcription factor?

Clue: they develop from the Th0

A

Treg

169
Q

What is X-linked Hyper-IgM syndrome?

A

Deficiency of IgG, IgA, and IgE and elevated levels of IgM.

IgM levels can reach 2,000 mg/dL (normal 45-250 mg/dL).
Most commonly inherited as X-linked recessive disorder but some form seem to be acquired and can be seen in both sexes.

Children with this condition suffer recurrent respiratory infections.

The defect in this syndrome is in the gene encoding the CD40 ligand which maps to the X chromosome. Therefore, Th cells in these patients will fail to express functional CD40L on their membrane, failing to give the costimulatory signal needed for the B-cell response to T-dependent antigens. As a result, only IgM antibodies are produced. The B-cell response to T-independent antigens is unaffected

170
Q

What is the predponderant isotope of immunoglobulin that begins to be produced after IgM during the primary immune response is ______.

A

IgG

171
Q

What are the 4 different subisotypes (subclasses) in humans?

A

IgG1, IgG2, IgG3, IgG4

172
Q

Which Ig can actively transport across the placenta by receptor mediated transport and thus plays a crucial role in protection of the fetus during gestation?

A

IgG

173
Q

Which Ig serves as a major protective defense of the mucosal surfaces of the body and what is its function?

A

IgA

Functions as a neutralizing antibody by inhibiting the binding of toxins or pathogens to the mucosa of the digestive, respiratory, and urogenital systems (sole function)

174
Q

What is the function of IgE?

A

Involved in elicitation of protective immune responses against parasites and allergens.

IgE is the antibody that binds to mast cells and is responsible for antihelminthic and allergic responses.

175
Q

What is the function of IgM?

A

The functions of IgM are (as a monomer) receptor on B cells, antigen capture in the secondary lymphoid organs, and (as a pentamer) in plasma, activation of complement.

176
Q

What is the function of IgG?

A

IgG is the major isotype produced after IgM. It exists in 4 subisotypes. It activates complement, opsonizes, mediates ADCC, and is actively transported across the placenta

177
Q

What is the function of IgA?

A

IgA is the major isotype produced in the submucosa, colostrum, and breast milk. It is a dimer with a J chain holding it together. It functions in inhibiting the binding of substances to cells or mucosal surfaces. It does not activate complement or mediate opsonization.

178
Q

Cell-mediated immunity has evolved to battle 2 different types of pathogens:

A

Facultative intracellular pathogens, which have adapted to living inside of phagocytic cells that are designed to kill them

Obligate intracellular pathogens, which can’t replicate outside of host cells

179
Q

Can IgM cross the placenta?

A

Nope

180
Q

What is an idiotype?

A

The unique pocket created by the variable regions of the light chain and the heavy chain is called the idiotype of the antibody.

It is the region that is specific for antigen. It is both extremely diverse and specific. Each individual is capable of producing hundreds of millions of unique idiotypes.

181
Q

What is an isotope?

A

The isotype of the antibody is determined by the constant region and is encoded by the heavy chain genes. The isotype of the antibody determines its function

182
Q

What is an allotype?

A

The allotype of an antibody is an allelic difference in the same antibody isotypes that differ between people. For example, 2 individuals with the same IgG have subtle differences in their immunoglobulins due to heterogeneity which tends to be specific for individuals. A patient receiving pooled gamma globulins might react to these allotypic differences in the constant regions which may result in type III hypersensitivity reactions.

183
Q

What is the difference between papain and pepsin digestion?

A

If an antibody molecule is digested with papain, cleavage occurs above the disul de bonds that hold the heavy chains together. This generates 3 separate fragments, two of which are called Fab (fragment antigen binding), and one of which is called Fc (fragment crystallizable).

Cleavage of the antibody molecule with pepsin generates one large fragment called F(ab ́)2 and a digested Fc fragment. The bridging of antigens by antibody molecules is required for agglutination of particulate antigens or the precipitation of soluble antigens.

184
Q

Agglutination and precipitation are maximized when multiple antibody molecules share the binding of multiple antigenic determinants, a condition known as ____________.

A

equivalence

185
Q

What is the mono spot test used for?

A

The mononuclear spot test or monospot test, a form of the heterophile antibody test, is a rapid test for infectious mononucleosis due to Epstein–Barr virus (EBV). It is an improvement on the Paul–Bunnell test.

186
Q

What is Coombs test used for?

A

Two variations of the Coombs test exist

The direct Coombs is designed to identify maternal anti-Rh antibodies that are already bound to infant RBCs or antibodies bound to RBCs in patients with autoimmune hemolytic anemia.

The indirect Coombs test is designed to identify Rh-negative mothers who are producing anti-Rh antibodies of the IgG isotype, which may be transferred across the placenta harming Rh-positive fetuses. The indirect Coombs is also used in the diagnosis of transfusion reactions.

187
Q

What is agglutination?

A

It is the clumping of particles. It is the process that occurs if an antigen is mixed with its corresponding antibody called isoagglutinin.

188
Q

What is the direct fluorescent antibody test (DFA)?

A

The direct fluorescent antibody test (DFA) is used to detect and localize antigen in the patient.

The tissue sample to be tested is treated with antibodies against that particular antigen that have been labeled with a fluorescent dye. If the antigen is present in the tissues, the fluorescent-labeled antibodies will bind, and their binding can be detected with a microscope.

Variations of this test are used to diagnose respiratory syncytial virus, herpes simplex 1 and 2, rabies in animal tissues, and Pneumocystis infections.

189
Q

What is the indirect fluorescent antibody test (IFA)?

A

The indirect fluorescent antibody test (IFA) is used to detect pathogen-specific antibodies in the patient.

In this case, a laboratory-generated sample of infected tissue is mixed with serum from the patient. A uorescent labeled anti-immunoglobulin is then added. If binding of antibodies from the patient to the tissue sample occurs, then the fluorescent antibodies can be bound and detected by microscopy. This technique can be used to detect autoantibodies in various autoimmune diseases.

190
Q

What is the Enzyme-linked Immunosorbent Assay (ELISA)?

A

It can be used to detect the presence of hormones, drugs, antibiotics, serum proteins, infectious disease antigens, and tumor markers. It does so by utilizing a chromogenic substrate that undergoes an enzyme-mediated color change.

191
Q

How is ELISA used in HIV?

A

In the screening test for HIV infection, the ELISA is used with the p24 capsid antigen coated onto microtiter plates.

192
Q

What is the Fluorescence activated cell sorting (FACS)?

A

Fluorescence activated cell sorting (FACS) of live cells separates a population of cells into sub-populations based on fluorescent labeling.

193
Q

Direct Coombs vs Indirect Coombs

A

The direct Coombs test is an agglutination test that detects infants at risk for developing erythroblastosis fetalis; the indirect Coombs test is used to diagnose the presence of antibody in mothers who are at risk of causing this condition in their children.

194
Q

What is Flow cytometry used for?

A

Flow cytometry is used to analyze and separate cell types out of complex mixtures.

195
Q

Who started the practice of vaccination?

A

The concept dates back into the 1100s when the Chinese practiced the art of variolation. However, the practice is credited to Edward Jenner in 1798, when he used a strain of cowpox virus to protect a child from smallpox.

196
Q

What are the 4 types of immunity?

A

Natural Passive
Natural Active
Artificial Passive
Artificial Active

197
Q

What type of immunity is this:

Placental IgG transport, colostrum

A

Natural Passive

198
Q

What type of immunity is this:

Horse antivenin against black widow spider bite, snake bite

A

Artificial Passive

199
Q

What type of immunity is this:

Hepatitis B component vaccine

A

Artificial Active

200
Q

What type of immunity is this:

Varicella attenuated vaccine

A

Artificial Active

201
Q

What type of immunity is this:

Recovery from infection

A

Natural Active

202
Q

What type of immunity is this:

Measles, mumps, rubella attenuated vaccine

A

Artificial Active

203
Q

What type of immunity is this:

Diphtheria, tetanus, pertussis toxoid vaccine

A

Artificial Active

204
Q

What type of immunity is this:

“Humanized” monoclonal antibodies versus RSV*

A

Artificial Passive

205
Q

What type of immunity is this:

Haemophilus capsular vaccine

A

Artificial Active

206
Q

What type of immunity is this:

Polio live or inactivated vaccine

A

Artificial Active

207
Q

What type of immunity is this:

Horse antitoxin against botulism, diphtheria

A

Artificial Passive

208
Q

What type of immunity is this:

Pooled human immune globulin versus hepatitis A and B, measles, rabies, varicella zoster or tetanus

A

Artificial Passive

209
Q

What is a live vaccine?

A

-Attenuated = weak
-Comprised of live organisms which lose capacity to cause disease but still replicate in the host
-Best at stimulating both a humoral and cell mediated immune response, as they mimic the natural infection and typically elicit lifelong immunity
– Typically, 1 dose provides immunity but 2 doses are used to ensure sero- conversion in most individuals
– Dangerous for immunocompromised patients because even attenuated viruses can cause them significant disease; since attenuated vaccines are comprised of live organisms, there is slight potential to revert back to a virulent form

210
Q

Examples of Live Viral vaccines in USA?

A 
Live viral vaccines:
o Recommended in the United States:
 Measles, mumps and rubella (MMR)
 Varicella zoster (VZV) (for both chicken pox and zoster [shingles])  Rotavirus
 Influenza (flu-mist)

o Available in the United States but recommended only under special circumstances:
 Polio (sabin)  Smallpox
 Yellow fever

211
Q

What is the only Non-attenuated vaccines used in the USA?

A

–Used by U.S. military against adenovirus types 4 and 7
– Enteric coated, live, non-attenuated virus preparation
– Produces an asymptomatic intestinal infection, thereby inducing mucosal IgA memory cells; these cells then populate the mucosal immune system throughout the body
– Vaccine recipients are thus protected against adenovirus acquired by aerosol, which could otherwise produce pneumonia (this is the only example of a live non-attenuated vaccine that is used)

212
Q

What is a killed vaccine?

A

Utilize organisms that are killed so they can no longer replicate in the host

Inactivated by chemicals rather than heat, as heat will often denature the
immunogenic epitopes

Typically require several doses to achieve desired response

Predominantly produce humoral immunity

213
Q

What are some examples of killed vaccines?

A

– Rabies
– Influenza
– Polio (Salk)
– Hepatitis A

214
Q

What is a toxoid vaccine?

A

Toxoid Vaccines
● Made from inactivated exotoxins from toxigenic bacteria
● Prevent disease but not infection
● Toxoid vaccines:
– Diphtheria, tetanus, and acellular pertussis (DTaP)*

215
Q

What is the DTaP vaccine?

A

The DTaP vaccine prep is composed of toxoids from both diphtheria and tetanus, while the pertussis is comprised of whole inactivated pertussis.

216
Q

What is a polysaccharide vaccine?

A

Comprised of the capsular polysaccharide found in many bacteria
● Are only capable of producing IgM because of the inability of polysaccharide to activate Th cells (which require protein to become activated)
● Have largely been replaced with conjugate vaccines (see below)

● Polysaccharide vaccine(s):
– Streptococcus pneumoniae, pneumococcal polysaccharide (PPSV23)

o Comprised of 23 capsular serotypes of the most invasive and common strains of S. pneumoniae

o Indicated for use in adults age >65 or special circumstances, i.e., spleenectomy, COPD

217
Q

What is a conjugate vaccine?

A

Comprised of capsular polysaccharide conjugated to protein (usually a toxoid (see figure I-10-3); this creates a T cell-dependent immune response with class switching
● Creates a booster response to multiple doses
● Conjugate vaccines:
– Haemophilus influenzae type b (Hib)
– Streptococcus pneumoniae, Pneumococcal conjugate (PCV13)
o Comprised of 13 capsular serotypes
o Indicated for use in infants
– Neisseria meningitidis

218
Q

What is a component vaccine?

A

Comprised of an immunodominant protein from the virus that is grown in yeast cells
– For example, in the hepatitis B vaccine, the gene coding for the HBsAg is inserted into yeast cells, which then releases this molecule into the cul- ture medium; the molecule is then purified and used as the immunogen in the vaccine
● Component vaccines: – HBV
o Hepatitis B surface antigen – HPV

219
Q

DEFECTS OF PHAGOCYTIC CELLS:

Molecular Defects and symptoms of:

Chronic Granulomatous Disease (CGD)

A

Molecular defect:
Deficiency of NADPH oxidase (any one of 4 component proteins); failure to generate superioxide ion, other O2 radicals

Symptoms:
Recurrent infections with catalase positive bacteria and fungi

220
Q

DEFECTS OF PHAGOCYTIC CELLS:

Molecular Defects and symptoms of:

Leukocyte Adhesion Deficiency (LAD)

A

Molecular defect:
Absence of CD18 - common B chain of the leukocyte integrins.
The 3 interns that contain CD18: LFA-1, MAC-1, and gp150/95

Symptoms:
Recurrent and chronic infections, failure to form pus and delayed separation of umbilical cord stump.

221
Q

DEFECTS OF PHAGOCYTIC CELLS:

Molecular Defects and symptoms of:

Chediak-Higashi syndrome

A

Molecular defect:
Nonsense mutation in the lysosomal trafficking regulator, CHS1/LYST protein, leads to aberrant fusion of vesicles

Symptoms:
Recurrent infection with bacteria: chemotactic and degranulation defects absent NK activity, partial albinism

222
Q

DEFECTS OF PHAGOCYTIC CELLS:

Molecular Defects and symptoms of:

Glucose-6-phospahate dehydrogenase (G6PD) deficiency

A

Molecular defect:
Deficiency of essential enzyme in hexose monophosphate shunt

Symptoms:
Same as CGD, with associated anemia.

Recurrent infections with catalase positive bacteria and fungi

223
Q

DEFECTS OF PHAGOCYTIC CELLS:

Molecular Defects and symptoms of:

Myeloperoxidase deficiency

A

Molecular defect:
Defect in MPO affects the ability to convert hydrogen peroxide to hypochlorite

Symptoms:
Mild or none

224
Q

DEFECTS OF PHAGOCYTIC CELLS:

Molecular Defects and symptoms of:

Hyperimmunoglobulin E syndrome

A

Molecular defect:
Defects in JAK-STAT signaling pathway leading to impaired Th17 function: decreased IFN-gamma production

Symptoms:

  1. Characteristic facies
  2. severe recurrent sinusopulmonary infections
  3. pathologic bone fractures
  4. retention of primary teeth
  5. increased IgE
  6. eczematous rash
225
Q

DEFECTS OF HUMORAL IMMUNITY:

Molecular defect:
Symptoms/signs:
Treatment:

BRtuon (X-linked) agammaglobulinemia

A

Molecular defect:
Deficiency of the Bruton tyrosine kinase (btk) which promotes pre-B cell expansions; faulty B-cell development.

Symptoms/signs:
Increased susceptibility to encapsulated bacteria and blood borne viruses, low immunoglobulins of all isotopes, absent or low levels of circulating B-cells.
B-cell maturation does not progress past the pre-B cell stage while maintaining cell-mediated immunity.

Treatment:
Monthly gamma-globlilun replacement, antibiotics for infections

226
Q

DEFECTS OF HUMORAL IMMUNITY:

Molecular defect:
Symptoms/signs:
Treatment:

X-linked hyper-IgM syndrome

A

Molecular defect:
Deficiency of CD40L on activated T cells

Symptoms/signs:
High serum titers of IgM without other isotopes, normal B and T-cell numbers, susceptibility to encapsulated bacteria and opportunistic pathogens.

Treatment:
Antibiotics and gammaglobulins

227
Q

DEFECTS OF HUMORAL IMMUNITY:

Molecular defect:
Symptoms/signs:
Treatment:

Selective IgA deficiency

A

Molecular defect:
Multiple Genetic causes

Symptoms/signs:
Decreased IgA levels and normal IgM and igG with elevation of IgE. Repeated sinopulmonary and gastrointestinal infections, increased atopy

Treatment:
Antibiotics, NOT immunoglobulins

228
Q

DEFECTS OF HUMORAL IMMUNITY:

Molecular defect:
Symptoms/signs:
Treatment:

Common variable Immunodeficiency

A

Molecular defect:
Collection of syndromes; several associated genetic defects.

Symptoms/signs:
Onset in late teens, early twenties,

Treatment:
antibiotics

229
Q

DEFECTS OF HUMORAL IMMUNITY:

Molecular defect:
Symptoms/signs:
Treatment:

Transient Hypogammaglobulinemia of infancy

A

Molecular defect:
Delayed onset of normal IgG synthesis

Symptoms/signs:
Detected in 5th to 6th month of life, resolves by 16-30 months; susceptibility to pyogenic bacteria

Treatment:
Antibiotics and in severe cases, gamma-globulin replacement.

230
Q

SELECTIVE T CELL DEFICIENCY:

Defect:
Clinical Manifestation:

DiGeorge Syndrome

A

Defect: Heterozygous deletion of chromosome 22q11. Failure of formation of 3rd and 4th paryngeal pouches, thymic aplasia

Clinical Manifestation: Characteristic facies and a clinical triad of cardiac malformations, hypocalcemia and hypoplastic thymus

231
Q

SELECTIVE T CELL DEFICIENCY:

Defect:
Clinical Manifestation:

MHC class I deficiency

A

Defect: Failure of TAP 1 molecules to transport peptides to endoplasmic reticulum

Clinical Manifestation: CD8+ T cells deficient, CD4+ T cells normal, recurring viral infections, normal DTH, normal Ab production

232
Q

COMBINED PARTIAL B AND T CELL DEFICIENCY:

Defect:
Clinical Manifestation:

Wiskott-Aldrich Syndrome

A

Defect: Defect in the WAS protein which plays a critical role in actin cytoskeleton rearrangement

Clinical Manifestation: Defective responses to bacterial polysaccharides and depressed IgM, gradual loss of humoral and cellular responses, thrombocytopenia, and eczema

IgA and IgE may be elevated.

Triad: thrombocytopenia, eczema, immunodeficiency

233
Q

COMBINED PARTIAL B AND T CELL DEFICIENCY:

Defect:
Clinical Manifestation:

Ataxia telangiectasia

A

Defect: Defect in the ATM kinase involved in the detection of DNA damage and progression through the cell cycle.

Clinical Manifestation: Ataxia (gait abnormalities), telangiectasia (capillary distortions in the eye), deficiency of IgA and IgE production

234
Q

COMPLETE PARTIAL B AND T CELL DEFICIENCY:

Defect:
Clinical Manifestation:

Severe combined immunodeficiency (SCID)

A

Defect: Defects in common Y chain of IL-2 receptor, X linked, Adenosine deaminase deficiency (Results in toxic metabolic products in cells), RAG1 and RAG2 gene nonsense mutations

Clinical Manifestation:
Chronic diahrrea; skin, mouth and throat lesions; opportunistic (fungal) infections; low levels of circulating lymphocytes; cells unresponsive to mitogens; clinical overall with X linked SCID plus neurologic deficiency, total absence of B + T cells

235
Q

COMPLETE PARTIAL B AND T CELL DEFICIENCY:

Defect:
Clinical Manifestation:

Bare lymphocyte syndrome/MHC class II deficiency

A

Defect: Failure of MHC class II expression, defects in transcription factors

Clinical Manifestation: T cells present and responsive to nonspecific mitongens, no GVHD, deficient in CD4+ T cells, hypogammaglobulinemia, Clinically observed as a severe combined immunodeficiency.

236
Q

What are the four types of hypersensitivity?

A
  1. Immediate (type I)
  2. Antibody-mediated (type II)
  3. Immune complex-mediated (type III)
  4. Delayed type hypersensitivity (type IV)
237
Q

Which type of hypersensitivity is this?

Immune Mechanism: Activation of Th2 cells resulting in the production of IgE which in turn binds to FCeR on mast cells, basophils and eosinophils

A

Immediate (type I)

238
Q

Which type of hypersensitivity is this?

Immune Mechanism: IgM and IgG against surface (cell surface or extracellular matrix)

A

Antibody mediated (type II)

239
Q

Which type of hypersensitivity is this?

Immune Mechanism: Deposition of immune complexes comprised of IgM or IgG and soluble antigen

A

Immune complex-mediated (type III)

240
Q

Which type of hypersensitivity is this?

Immune Mechanism: Inflammatory cytokines, IGN-y and IL-17, produced by CD4+ Th1 and Th17 cells, respectively

A

Delayed-type hypersensitivity (type IV)

241
Q

What is an atopic response?

A

Approximately 20% of all individuals in the United States, however, display this immune response against harmless environmental antigens, such as pet dander or pollen; these responses are called atopic or allergic responses.

242
Q

What is the effect of Histamine?

A

Smooth muscle contraction; increased vascular permeability.

243
Q

What is the effect of heparin?

A

anticoagulant

244
Q

What is the effect of eosinophil chemotactic factor A (multiple chemokines)?

A

Chemotactic

245
Q

What is the effect of prostaglandin D2, E2, F2a?

A

Increased smooth muscle contraction and vascular permeability.

246
Q

What is the effect of Leukotrienes C4, D4, E4 (lipoxygenase pathway)?

A

Increased smooth muscle contraction and vascular permeability.

247
Q

What is the effect of Leukotriene B4?

A

Chemotactic for neutrophils

248
Q

ALLERGIC DISEASE:

Allergens:
Clinical Findings:

Allergic Rhinitis (hay fever)

A

Allergens: Trees, grasses, dust, cats, dogs, mites

Clinical Findings: Edema, irritation, mucus un nasal mucosa

249
Q

ALLERGIC DISEASE:

Allergens:
Clinical Findings:

Systemic anaphylaxis

A

Allergens: Insect stings, drug reactions

Clinical Findings: Bronchial and tracheal constriction, complete vasodilation and death

250
Q

ALLERGIC DISEASE:

Allergens:
Clinical Findings:

Food allergies

A

Allergens: Milk, eggs, fish, cereal grains

Clinical Findings: Hives and gastrointestinal problems

251
Q

ALLERGIC DISEASE:

Allergens:
Clinical Findings:

Wheal and flare

A

Allergens: In vivo skin testing for allergies

Clinical Findings: Local skin edema, redding, vasodilation of vessels

252
Q

ALLERGIC DISEASE:

Allergens:
Clinical Findings:

Asthma

A

Allergens: Inhaled materials

Clinical Findings: Bronchial and tracheal constriction, edema, mucus production, massive inflammation

253
Q

TYPE II HYPERSENSITIVITIES: CYTOTOXIC

Target antigen:
Mechanism of Pathogenesis:
Clinical Manifestation:

Autoimmune hemolytic anemia (HDNB) AKA erythroblastosis fetalis

A

Target antigen: RBC membrane proteins (Rh, I Ags)

Mechanism of Pathogenesis: Opsonization, phagocytosis, and complement-mediated destruction of RBCs

Clinical Manifestation: Hemolysis, anemia

254
Q

TYPE II HYPERSENSITIVITIES: CYTOTOXIC

Target antigen:
Mechanism of Pathogenesis:
Clinical Manifestation:

Acute rheumatic fever

A

Target antigen: Streptococcal cell-wall Ag; Ab cross0reacts with myocardial Ag

Mechanism of Pathogenesis: Inflammation, macrophage activation

Clinical Manifestation: Myocarditis, arthritis

255
Q

TYPE II HYPERSENSITIVITIES: CYTOTOXIC

Target antigen:
Mechanism of Pathogenesis:
Clinical Manifestation:

Goodpasture syndrome

A

Target antigen: Type IV collagen in basement membranes of kidney glomeruli and lung alveoli

Mechanism of Pathogenesis: Complement and Fc receptor mediated inflammation

Clinical Manifestation: Nephritis, lung hemorrhage, linear Ab deposits

256
Q

TYPE II HYPERSENSITIVITIES: CYTOTOXIC

Target antigen:
Mechanism of Pathogenesis:
Clinical Manifestation:

Transfusion reaction

A

Target antigen: ABO blood Glycoproteins

Mechanism of Pathogenesis: IgM isohemagglutinins formed naturally in response to normal bacteria flora cause opsonization + complement activation

Clinical Manifestation: Hemolysis

257
Q

TYPE II HYPERSENSITIVITIES: CYTOTOXIC

Target antigen:
Mechanism of Pathogenesis:
Clinical Manifestation:

Autoimmune thrombocytopenia purpura

A

Target antigen: Platelet membrane proteins

Mechanism of Pathogenesis: Ab-mediated platelet destruction through opsonization and complement activation

Clinical Manifestation: bleeding

258
Q

TYPE II HYPERSENSITIVITIES: NON-CYTOTOXIC

Target antigen:
Mechanism of Pathogenesis:
Clinical Manifestation:

Myasthenia gravis

A

Target antigen: Acetylcholine receptor

Mechanism of Pathogenesis: Ab inhibits actual choline binding, down modulates receptors

Clinical Manifestation: Muscle weakness, paralysis

259
Q

TYPE II HYPERSENSITIVITIES: NON-CYTOTOXIC

Target antigen:
Mechanism of Pathogenesis:
Clinical Manifestation:

Graves disease

A

Target antigen: TSH receptor

Mechanism of Pathogenesis: AB mediated stimulation of TSH receptors

Clinical Manifestation: Hyperthyroidism filled by hypothyroidism

260
Q

TYPE II HYPERSENSITIVITIES: NON-CYTOTOXIC

Target antigen:
Mechanism of Pathogenesis:
Clinical Manifestation:

Type II (insulin-resistant) diabetes

A

Target antigen: Insulin receptor

Mechanism of Pathogenesis: Ab inhibits binding of insulin

Clinical Manifestation: Hyperglycemia

261
Q

TYPE II HYPERSENSITIVITIES: NON-CYTOTOXIC

Target antigen:
Mechanism of Pathogenesis:
Clinical Manifestation:

Pernicious anemia

A

Target antigen: Intrinsic factor of gastric parietal cells

Mechanism of Pathogenesis: Neutralization of intrinsic factor, decreased absorption of vitamin B12

Clinical Manifestation: Abnormal erythropoiesis, anemia

262
Q

Pathogenesis of Autoimmune hemolytic anemia (HDNB) AKA erythroblastosis fetalis:

A

An important example of type II hypersensitivity is HDNB, also known as erythro- blastosis fetalis. In the fetus, this disease is due to transport of IgG speci c for one of the Rhesus (Rh) protein antigens (RhD) across the placenta.

About 85% of people are Rh+. If a pregnant woman is Rh– and the father is Rh+, there is a chance that the fetus will also be Rh+. is situation will pose no problem in the rst pregnancy, as the mother’s immune system will not usually encounter fetal blood cell antigens until placental separation at the time of birth. At that time, however, Rh+ fetal red blood cells will enter the maternal circulation and stimulate a T-dependent immune response, eventually resulting in the generation of memory B cells capable of producing IgG antibody against RhD.

In a subsequent pregnancy with another Rh+ fetus, this maternal IgG can be trans- ported across the placenta, react with fetal Rh+ red cells, and activate complement, producing hemolytic disease. Hemolytic disease of the newborn can be prevented by treating the Rh– mother with RhoGAMTM, a preparation of human anti-RhD anti- body, at 28 weeks of gestation and again within 72 hours a er birth. is antibody ef- fectively eliminates the fetal Rh+ cells before they can generate RhD-speci c memory B cells in the mother. Anti-RhD antibody should be given to any Rh– individual fol- lowing any termination of pregnancy.

263
Q

TYPE III HYPERSENSITIVITIES:

Antigen Involved:
Clinical Manifestations:

Systemic Lupus Erythematosus

A

Antigen Involved: dsDNA, Sm, other nucleoproteins

Clinical Manifestations: Nephritis, arthritis, vasculitis, butterfly facial rash

264
Q

TYPE III HYPERSENSITIVITIES:

Antigen Involved:
Clinical Manifestations:

Poststreptococcal glomerulonephritis

A

Antigen Involved: Streptococcal cell wall Ags (may be “planted” in glomerular basement membrane)

Clinical Manifestations: Nephritis, “lumpy-bumpy” deposits

265
Q

TYPE III HYPERSENSITIVITIES:

Antigen Involved:
Clinical Manifestations:

Arthus reaction

A

Antigen Involved: Any injected protein

Clinical Manifestations: Local pain and edema

266
Q

TYPE III HYPERSENSITIVITIES:

Antigen Involved:
Clinical Manifestations:

Serum sickness

A

Antigen Involved: Various proteins

Clinical Manifestations: Arthritis, vasculitis, nephritis

267
Q

TYPE III HYPERSENSITIVITIES:

Antigen Involved:
Clinical Manifestations:

Polyarteritis nodosa

A

Antigen Involved: Hepatitis B virus Ag

Clinical Manifestations: Systemic vasculitis

268
Q

What kind of hypersensitivity is this?

T lymphocytes may cause tissue injury by triggering delayed-type hypersensitivity (DTH) reactions or by directly killing target cells. These reactions are elicited by CD4+ 1, 17 cells, or CD8+ CTLs, which activate macrophages, recruit neutrophils, and induce inflammation. These T cells may be autoreactive or specific against foreign protein antigens bound to tissues

A

Type IV (T-cell mediated) hypersensitivity

269
Q

TYPE IV HYPERSENSITIVITIES:

Specificity of Pathogenic T cells:
Clinical manifestations:

Tuberculin test

A

Specificity of Pathogenic T cells: PPD (tuberculin & mycolic acid

Clinical manifestations: Indurated skin lesion (granuloma)

270
Q

TYPE IV HYPERSENSITIVITIES:

Specificity of Pathogenic T cells:
Clinical manifestations:

Contact dermatitis

A

Specificity of Pathogenic T cells: Nickel, poison ivy/oak catechols, happen/carrier

Clinical manifestations: Vesicular skin lesions, pruritus, rash

271
Q

TYPE IV HYPERSENSITIVITIES:

Specificity of Pathogenic T cells:
Clinical manifestations:

Hashimoto Thyroiditis

A

Specificity of Pathogenic T cells: Unknown Ag in thyroid

Clinical manifestations: Hypothyroidism

272
Q

TYPE IV HYPERSENSITIVITIES:

Specificity of Pathogenic T cells:
Clinical manifestations:

Multiple sclerosis

A

Specificity of Pathogenic T cells: Myelin Basic Protein

Clinical manifestations: Progressive demyelination, blurred vision, paralysis

273
Q

TYPE IV HYPERSENSITIVITIES:

Specificity of Pathogenic T cells:
Clinical manifestations:

Rheumatoid arthritis

A

Specificity of Pathogenic T cells: Unknown Ag in Joint synovium (type II collagen?)

Clinical manifestations: Rheumatoid factor (IgM against Fc region of IgG), alpha-cyclic citrullinated peptide (a-CCP) antibodies, chronic arthritis, inflammation, destruction of articular cartilage and bone

274
Q

TYPE IV HYPERSENSITIVITIES:

Specificity of Pathogenic T cells:
Clinical manifestations:

Insulin-Dependent diabetes mellitus (type I)

A

Specificity of Pathogenic T cells: Islet cell antigens, insulin, glutamic acid decarboxylase, others

Clinical manifestations: Chronic inflammation and destruction of B cells, polydipsia, polyuria, polyphagia, ketoacidosis

275
Q

TYPE IV HYPERSENSITIVITIES:

Specificity of Pathogenic T cells:
Clinical manifestations:

Guillain Barre syndrome

A

Specificity of Pathogenic T cells: Peripheral nerve myelin or gangliosides

Clinical manifestations: Ascending paralysis, peripheral nerve demyelination

276
Q

TYPE IV HYPERSENSITIVITIES:

Specificity of Pathogenic T cells:
Clinical manifestations:

Celiac disease

A

Specificity of Pathogenic T cells: CD4+ cells - gliadin, CD8+ cells -HLA class I-like molecule expressed during stress

Clinical manifestations: Gluten-sensitive enteropathy

277
Q

TYPE IV HYPERSENSITIVITIES:

Specificity of Pathogenic T cells:
Clinical manifestations:

Crohn disease

A

Specificity of Pathogenic T cells: Unknown Ag, commensal bacteria?

Clinical manifestations: Chronic intestinal inflammation due to Th1 and Th17 cells, obstruction

278
Q

HLA-linked Immunologic Disease:

HLA Allele:

Rheumatoid Arthritis

A

HLA Allele: DR4

279
Q

HLA-linked Immunologic Disease:

HLA Allele:

Insulin-dependent diabetes mellitus

A

HLA Allele: DR3/DR4

280
Q

HLA-linked Immunologic Disease:

HLA Allele:

Multiple sclerosis, Goodpasture’s

A

HLA Allele: DR2

281
Q

HLA-linked Immunologic Disease:

HLA Allele:

Systemic lupus erythematosus

A

HLA Allele: DR2/DR3

282
Q

HLA-linked Immunologic Disease:

HLA Allele:

Ankylosing spondylitis, psoriasis, inflammatory bowel disease, reactive arthritis

A

HLA Allele: B27

283
Q

HLA-linked Immunologic Disease:

HLA Allele:

Celiac disease

A

HLA Allele: DQ2 or DQ8

284
Q

HLA-linked Immunologic Disease:

HLA Allele:

Graves disease

A

HLA Allele: B8

285
Q

What type of hypersensitivities involve IgE antibodies and mast cells, show symptoms in minutes, and are mounted against harmless environmental antigens in atopic or allergic individuals.

– Initial tissue damage in immediate hypersensitivities is due to release of mast cell mediators, and late-phase reactions involve products of the arachidonic acid cascade.
– Examples include hay fever, asthma, food allergies, and systemic anaphylaxis.

A

Type I hypersensitivities (immediate) hypersensitivities

286
Q

What type of hypersensitivity are tissue-specific and involve autoantibodies that opsonize or activate complement. Some noncytotoxic forms (myasthenia gravis, Graves disease, type II diabetes) cause interference with cellular function.

– Examples (cytotoxic) include autoimmune hemolytic anemia, hemolytic disease of the newborn, autoimmune thrombocytopenic purpura, Goodpasture syndrome, rheumatic fever, and pernicious anemia.

A

Type II (antibody-mediated) hypersensitivities

287
Q

What type of hypersensitivity cause systemic damage by activating complement wherever immune complexes of antibodies against self or foreign antigens are filtered from the circulation.
– Examples include systemic lupus erythematosus, polyarteritis nodosa, poststreptococcal glomerulonephritis, serum sickness, and the Arthus reaction.

A

Type III (immune complex) hypersensitivities

288
Q

What type of hypersensitivity are delayed-type (manifesting symptoms 48-72 hrs after reexposure); are caused by TH1 and TH17 cells, CD8+ cells, and macrophages; and are common results of infection with persistent intracellular microbes.

– Examples include the tuberculin test, insulin-dependent diabetes mellitus, celiac disease, contact dermatitis, Guillain-Barré syndrome, RA, Crohn disease and Hashimoto thyroiditis.

A

Type IV hypersensitivities

289
Q

It is the process of taking cells, tissues, or organs (a graft) from one individual (the donor) and implanting them into another individual or another site in the same individual (the host or recipient).

A

Transplantation

290
Q

It is a special case of transplantation and the most frequently practiced today, in which circulating blood cells or plasma are infused from one individual into another.

A

Transfusion

291
Q

Which type of graft are those where tissue is moved from one location to another in the same individual (skin grafting in burns or coronary artery replacement with saphenous veins)?

A

Autologous grafts (or autografts)

292
Q

Which type of graft are those transplanted between genetically identical individuals (monozygotic twins)?

A

Isografts (or syngeneic grafts)

293
Q

Which type of graft are those transplanted between genetically different members of the same species (kidney transplant)?

A

Allogeneic grafts

294
Q

Which type of grafts are those transplanted between members of different species (pig heart valves into human)?

A

Xenogeneic grafts

295
Q

What kind of graft rejection is this:

Occurs within minutes to hours
● Due to pre-formed antibodies due to transfusions, multi-parity, or previous
organ transplants (type II cytotoxic hypersensitivity)
● Antibodies bind to the grafted tissue and activate complement and the clot- ting cascade resulting in thrombosis and ischemic necrosis
● Rare because of cross-matching blood, but common vignette

A

Hyperacute Graft Rejection

296
Q

What kind of graft rejection is this:

Occurs within days to weeks; the timing and mechanism are similar to a primary immune response
● Induced by alloantigens (predominantly MHC) in the graft
● Both CD4 and CD8 T cells play a role as well as antibodies (think normal
immune response)
● Immunosuppressive therapy works to prevent this type of graft rejection mainly

A

Acute Graft Rejection

297
Q

What kind of graft rejection is this:

Occurs within days; the timing and mechanism are similar to a memory response.

A

Accelerated Acute Graft Rejection

298
Q

What kind of graft rejection is this:

● Occurs within months to years
● Predominantly T cell mediated
● Difficult to treat and usually results in graft rejection
● Etiology not well understood, possibly triggered by viral infections

A

Chronic Graft Rejection

299
Q

Monoclonal antibodies are used in the treatment and prevention of graft rejection along with the classic therapies (corticiosteroids, cyclosporine A, rapamycin, etc.). Several monoclonals currently in use for graft rejection are listed below.

Mechanism of Action:

Daclizumab, basiliximab (anti-IL-2 receptor antibody)

A

Mechanism of Action: Blocks T cell proliferation via blocking the binding of IL-2, opsonization of IL-2R bearing cells

300
Q

Monoclonal antibodies are used in the treatment and prevention of graft rejection along with the classic therapies (corticiosteroids, cyclosporine A, rapamycin, etc.). Several monoclonals currently in use for graft rejection are listed below.

Mechanism of Action:

Muromonab (anti-CD3)

A

Mechanism of Action: Blocks T cell activation by causing apoptosis

301
Q

Monoclonal antibodies are used in the treatment and prevention of graft rejection along with the classic therapies (corticiosteroids, cyclosporine A, rapamycin, etc.). Several monoclonals currently in use for graft rejection are listed below.

Mechanism of Action:

Belatacept (CTLA-4-Ig)

A

Mechanism of Action: Inhibits T cell activation by blocking the B7 costimulatory molecule binding to CD28

302
Q

Monoclonal antibodies are used in the treatment and prevention of graft rejection along with the classic therapies (corticiosteroids, cyclosporine A, rapamycin, etc.). Several monoclonals currently in use for graft rejection are listed below.

Mechanism of Action:

Alemtuzumab (anti-CD52)

A

Mechanism of Action: Depletes pool of T cells by binding to them and causing complement mediated lysis

303
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD2 (LFA-2)

A

Cellular Expression: T-cells, thymocytes, NK cells

Known Functions: Adhesion molecule

304
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD3

A

Cellular Expression: T cells, thymocytes

Known Functions: Signal transduction by the TCR

305
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD4

A

Cellular Expression: Th cells, thymocytes, monocytes, and macrophages

Known Functions: Coreceptor for TCR-MHC II interaction, receptor for HIV

306
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD8

A

Cellular Expression: CTLs, some thymocytes

Known Functions: Coreceptor for MHC class I-restricted T cells

307
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD14 (LPS receptor)

A

Cellular Expression: monocytes, macrophages, granulocytes

Known Functions: Binds LPS

308
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD16 (Fc receptor)

A

Cellular Expression: NK cells, macrophages, neutrophils

Known Functions: Opsonization ADCC

309
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD18

A

Cellular Expression: Leukocytes

Known Functions: Cell adhesion molecule (missing in leukocyte adhesion deficiency

310
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD 19

A

Cellular Expression: B cells

Known Functions: Coreceptor with CD21 for B cell activation (signal transduction)

311
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD20

A

Cellular Expression: Most or all B cells

Known Functions: Unknown role in B cell activation

312
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD21 (CR2, C3d receptor)

A

Cellular Expression: Mature B cells

Known Functions: Receptor for complement fragment C3d, forms coreceptor complex with CD19, Epstein-Barr virus receptor

313
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD25

A

Cellular Expression: Activated Th cells and Treg

Known Functions: Alpha chain of IL-2 receptor

314
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD28

A

Cellular Expression: T cells

Known Functions: T-cell receptor for costimulatory molecule B7

315
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD34

A

Cellular Expression: Precursors of hematopoietic cells, endothelial cells in HEV

Known Functions: Cell-cell adhesion, binds L-selectin

316
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD40

A

Cellular Expression: B cells, macrophages, dendritic cells, endothelial cells

Known Functions: Binds CD40L, role in T-cell–dependent B cell, macrophage, dendritic cell and endothelial cell activation

317
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD56

A

Cellular Expression: NK cells

Known Functions: Cell adhesion

318
Q

CD MAKERS:

Cellular Expression:
Known Functions:

CD152 (CTLA-4)

A

Cellular Expression: Activated T cells

Known Functions: Negative regulation: competes with CD28 for B7 binding

319
Q

CYTOKINES AVAILABLE IN RECOMBINANT FORM:

Clinical uses:

Aldesleukin (IL-2)

A

Clinical uses:

↑ lymphocyte differentiation and ↑ NKs—used in renal cell cancer and metastatic melanoma

320
Q

CYTOKINES AVAILABLE IN RECOMBINANT FORM:

Clinical uses:

Interleukin-11

A

Clinical uses:

↑ platelet formation—used in thrombocytopenia

321
Q

CYTOKINES AVAILABLE IN RECOMBINANT FORM:

Clinical uses:

Filgrastim (G-CSF)

A

Clinical uses:

↑ granulocytes—used for marrow recovery

322
Q

CYTOKINES AVAILABLE IN RECOMBINANT FORM:

Clinical uses:

Sargramostim (GM-CSF)

A

Clinical uses:

↑ granulocytes and macrophages—used for marrow recovery

323
Q

CYTOKINES AVAILABLE IN RECOMBINANT FORM:

Clinical uses:

Erythropoietin

A

Clinical uses:

Anemias, especially associated with renal failure

324
Q

CYTOKINES AVAILABLE IN RECOMBINANT FORM:

Clinical uses:

Thrombopoietin

A

Clinical uses:

Thrombocytopenia

325
Q

CYTOKINES AVAILABLE IN RECOMBINANT FORM:

Clinical uses:

Interferon-α

A

Clinical uses:

Hepatitis B and C, leukemias, melanoma

326
Q

CYTOKINES AVAILABLE IN RECOMBINANT FORM:

Clinical uses:

Interferon-β

A

Clinical uses:

Multiple sclerosis

327
Q

CYTOKINES AVAILABLE IN RECOMBINANT FORM:

Clinical uses:

Interferon-γ

A

Clinical uses:

Chronic granulomatous disease →↑ TNF

KAPLAN - Immunology (1 decks)

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