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STEP > Immunology > Flashcards

Immunology Flashcards

1
Q

Positive selection location

A

thymic cortex

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2
Q

Negative selection location

A

Thymic medulla

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3
Q

MHC class II deficiency

A

/defect in development of CD4+ cells in the thymus. /no MHC class II so helper cells cannot be selected by positive selection mechanisms in the thymus but CD8 cytotoxic cells can be produced. /also known as type II bare lymphocyte syndrome.

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4
Q

Positive selection mechanism

A

T cells expressing TCRs capable of binding self-MHC on cortical epithelial cells survive.

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5
Q

Negative selection mechanism

A

T cells expressing TCRs with high affinity for self antigens undergo apoptosis. Tissue-restricted self-antigens are expressed in the thymus due to the action of autoimmune regulator (AIRE).

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6
Q

Autoimmune polyendocrine syndrome-1

A

deficiency of negative selection.

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7
Q

Lymph drainage of head and neck

A

cervical

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8
Q

Mediastinal lymp nodes drain

A

trachea and esophagus

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9
Q

Axillary lymph node drainage

A

Upper limb, breast, skin above umbilicus

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10
Q

Celiac lymph node drainage

A

Liver + stomach + spleen + pancreas + upper duodenum

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11
Q

Superior mesenteric lymph node drainage

A

lower duodenum + jejunum + ileum + colon to splenic flexure

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12
Q

Inferior mesenteric lymph node drainage

A

Colon from splenic flexure to upper rectum

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13
Q

Internal iliac drains

A

Lower rectum to anal canal (above pectinate line) + bladder + vagina (middle third) + cervix + prostate

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14
Q

Para-aortic drains

A

testes + ovaries + kidneys + uterus

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15
Q

Superficial inguinal node drains..

A

anal canal (below pectinate) + skin below umbilicus (except popliteal area) + scrotum + vulva.

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16
Q

popliteal drains

A

dorsolateral foot + posterior calf

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17
Q

thoracic duct drains into..

A

junction of left subclavian + internal jugular veins

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18
Q

Function of medullary sinus of lymph node

A

Outside near capsule. Houses reticular cells and macrophages, which perform nonspecific filtration.

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19
Q

Location of B-cells in lymph node

A

Outer cortex.

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20
Q

lymph node follicle

A

Site of b-cell localization and proliferation

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21
Q

Difference between primary follicles and secondary follicles.

A

Primary follicles are dense and dormant, secondary follicles are activated and have pale central germinal centers.

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22
Q

Function of medulla of lymph node and composition

A

Consists of medullary cords and medullary sinuses.

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23
Q

Medullary cords

A

Closely packed lymphocytes and plasma cells.

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24
Q

medullary sinuses

A

Communicate with efferent lymphatics and contain reticular cells and macrophages.

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25
Q

Where are T cells located in lymph node?

A

paracortex

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26
Q

Paracortex

A

region between follicles and medulla. Contains high endothelial venules through which T and B cells enter from blood.

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27
Q

Sinusoids of spleen

A

Long, vascular channels in red pulp with fenestrated “barrel hoop” basement membrane.

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28
Q

Where are T cells found in the spleen?

A

periarteriolar lymphatic sheath (PALS) within the white pulp.

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29
Q

Where are B cells found in the spleen?

A

Follicles within the white pulp.

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30
Q

Marginal zone of spleen.

A

Zone between the red pulp and white pulp that contains macrophages and specialized B cells.

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31
Q

Marginal zone of spleen function

A

Where APCs capture blood-borne antigens for recognition by lymphocytes.

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32
Q

GBS encapsulated or nonecapsulated?

A

encapsulated

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33
Q

Mechanism for increased susceptibility to encapsulated organisms with splenic dysfunction

A

Decreased IgM –> decreased complement activation –> decreased C3b opsonization.

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34
Q

Postsplenectomy hematologic findings

A

1) Howell-Jolly bodies (nuclear remnants)
2) Target cells
3) Thrombocytosis (loss of sequestration and removal)
4) lymphocytosis (loss of sequestration).

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35
Q

Spleen follicle organization

A

Germinal center surrounded by mantle zone surrounded by marginal zone.

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36
Q

Thymus location

A

Anterosuperior mediastinum

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37
Q

Thymus organization

A

Cortex is dense with immature T cells; medulla is pale with mature T cells and Hassall corpuscles

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38
Q

Hassall corpuscles

A

Contain epithelial reticular cells

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39
Q

T cell and B cell origin

A

T cells = Thymus (mature in thymus, originate in bone marrow), B cells = Bone marrow.

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40
Q

Thymic hypertrophy seen in…

A

MG

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41
Q

Innate immunity components

A

Neutrophils, macrophages, monocytes, dendritic cells, NK cells (lymphoid origin), complement.

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42
Q

Mechanism of innate immunity

A

Germline encoded

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43
Q

What physical barriers does innate immunity have?

A

epithelial tight junctions + mucus

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44
Q

Proteins secreted by innate immunity

A

lysozyme, complement, CRP, defensins.

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45
Q

Key features of pathogen recognition in innate immunity

A

Toll-like receptors (TLRs).

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46
Q

TLRs

A

Pattern recognition receptors that recognize pathogen-associated molecular patterns (PAMPs) (eg LPs, flagellin, nucleic acids (viruses))

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47
Q

Components of adapative immunity

A

T cells, B cells, circulating antibodies

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48
Q

MHC 1 loci

A

HLA-A, HLA-B, HLA-C (all have 1 letter)

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49
Q

MHC 1 expression

A

Expressed on all nucleated cells. Not expressed on RBCs.

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50
Q

MHC I vs. MHC II function

A

MHC 1 present endogenously synthesized antigens (eg viral or cytosolic proteins) to CD8+ T cells. MHC II prsent exogenously synthesized antigens (eg bacterial proteins to CD4+ helper T cells).

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51
Q

protein associated with MHC 1

A

Beta2-microglobulin

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52
Q

Antigen loading in MHC 1

A

Antigen peptides loaded onto MHC I in RER after delivery via TAP (transporter associated with antigen processing).

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53
Q

MHC II loci

A

HLA-DP, HLA-DQ, HLA-DR (all have 2 letters)

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54
Q

MHC II expression

A

Expressed on APCs

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55
Q

protein associated with MHC II

A

Invariant chain

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56
Q

Mechanism of MHC II

A

Antigen loaded following release of invariant chain in an acidified endosome.

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57
Q

HLA A3

A

hemochromatosis

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58
Q

Addison disease HLA association

A

B8

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59
Q

MG HLA association

A

B8

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60
Q

MS HLA association

A

DR2

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61
Q

RA HLA association

A

DR4

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62
Q

Addison’s HLA association

A

DR3 + DR4

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63
Q

Hashimoto’s HLA association

A

DR5

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64
Q

DM1 HLA association

A

DR3 + DR4

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65
Q

MS HLA association

A

DR2

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66
Q

Goodpasture’s HLA association

A

DR2

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67
Q

SLE HLA association

A

DR2 + DR3

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68
Q

Pernicious anemia HLA association

A

DR5

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69
Q

Hay fever HLA association

A

DR2

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70
Q

Graves HLA association

A

DR3

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71
Q

NK cell mechanism

A

Use perforin and granzymes to induce apoptosis of virally infected cells and tumor cells

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72
Q

What enhances NK cell activity?

A

IL-2 + IL-12 + IFN-alpha + IFN-beta

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73
Q

What induces NK cells?

A

Exposure to a nonspecific activation signal on target cell and/or to an absence of class I MHC on target cell surface.

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74
Q

NK cell other mechanism

A

antibody-dependent cell mediated cytotoxicity

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75
Q

antibody-dependent cell mediated cytotoxicity mechanism

A

CD16 binds Fc region of bound Ig, activating NK cell

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76
Q

Process of B cell antigen specificity

A

somatic hypermutation

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77
Q

CD4+ vs. CD8+ cells

A

CD4 help b cells make antibodies and produce cytokines to recruit phagocytes and activate other leukocytes. CD8 directly kill virus-infected cells.

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78
Q

Where are mature and immature T cells found?

A

immature in cortex, mature in medulla.

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79
Q

What activates Th1 cells?

A

IL-12

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80
Q

What activates Th2 cells?

A

IL-4

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81
Q

What activates Th17 cells?

A

TGF-beta + IL-6

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82
Q

What are cytotoxic T cells activated by?

A

Th1 cells

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83
Q

What induces differentiation of Th1 cells?

A

IFN-gamma and IL-12

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84
Q

What inhibits TH1 cells?

A

IL-4 + IL-10 (from Th2 cell)

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85
Q

What do Th2 cells secrete?

A

IL-4, IL-5, IL-10, IL-13

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86
Q

Th2 cell function

A

Recruit eosinophils for parasite defense and promote IgE production by B cells

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87
Q

What induces differentiation of Th2 cells?

A

IL-4

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88
Q

What inhibits Th2 cells?

A

IFN-gamma from Th1 cells

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89
Q

macrophage-lymphocyte interaction mechanism

A

Macrophages and other APCs release IL-12, which stimulates T cells to differentiate into Th1 cells. Th1 cells release IFN-gamma to stimulate macrophages.

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90
Q

Cytotoxic T cell mechanism

A

1) kill virus-infected, neopalstic, and donor graft cells by inducing apoptosis.
2) release cytotoxic granules containing preformed proteins (eg perforin, granzyme B)

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91
Q

Regulatory T cell mechanism

A

Maintain specific immune tolerance by suppressing CD4 and CD8 T-cell effector functions.

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92
Q

Regulatory T cell markers

A

CD3, CD4, CD25, FOXP3

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93
Q

What do activated regulatory T cells produce?

A

anti-inflammatory cytokines (IL-10 + TGF-beta)

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94
Q

APCs

A

B cells + macrophages + dendritic cells

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95
Q

Caveat about T and B cell activation

A

Two signals are required for T-cell activation, B-cell activation, and class switching.

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96
Q

Naive T-cell activation

A

Dendritic cell samples and processes antigen –> dendritic cell migrates to draining lymph node –> T-cell activation (signal 1): antigen is presented on MHC II and recognized by TCR on Th (CD4+) cell. Endogenous antigen is presented on MHC I to Tc (CD8+) cell –> Proliferation and survival (signal 2): costimulatory signal via interaction of B7 proteins (CD80/86) and CD28 –> Th cell activates and produces cytokines. Tc cell activates and is able to recognize and kill virus-infected cell.

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97
Q

B-cell activation and class switching mechanism

A
  1. Th-cell activation.
  2. B-cell receptor-mediated endocytosis; foreign antigen is presented on MHC II and recognized by TCR on Th cell.
  3. CD40 receptor on B cell binds CD40 ligand (CD40L) on Th cell.
  4. Th cell secretes cytokines that determine Ig class switching of B cell. B cell activates and undergoes class switching, affinity maturation, and antibody production.
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98
Q

Fab

A

region of antibody containing variable/hypervariable regions.

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99
Q

What fixes comploment

A

Fc region of IgM and IgG

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100
Q

Idiotype

A

unique antigen-binding pocket; only 1 antigenic specificity expressed per B cell.

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101
Q

carbohydrate side chains

A

Expressed on Fc region

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102
Q

What determines isotype (IgM, IgD, etc)?

A

Fc region

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103
Q

neutralization

A

Antibody binding and preventing bacterial adherence.

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104
Q

VJ

A

light-chain genes

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105
Q

V(D)J

A

heavy-chain genes

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106
Q

How is antibody diversity generated?

A

1) Random recombination of VJ (light-chain) or V(D)J (heavy-chain) genes.
2) random addition of nucleotides to DNA during recombination by terminal deoxynucleotidyl transferase (TdT)
3) Random combination of heavy chains with light chains

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107
Q

How is antibody specificity achieved?

A

1) Somatic hypermutation and affinity maturation (variable region)
2) Isotype switching (constant region)

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108
Q

Affinity maturation mechanism

A

Process by which Th cell-activated B cells produce antibodies with increased affinity for antigen. With repeated exposures to the same antigen, host produces antibodies of successively greater affinities.

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109
Q

Immunoglobulins expressed on mature, naive B cells prior to activation…

A

IgM and IgD

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110
Q

What mediates isotype switching?

A

CD40L and cytokines

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111
Q

Immunoglobulin responsible for neutralizing bacterial toxins and viruses

A

IgG

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112
Q

Main antibody in secondary (delayed) response to an antigen

A

IgG

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113
Q

Which immunoglobulins have J chains?

A

IgA and IgM

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114
Q

IgA in circulation

A

Exists as a monomer

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115
Q

How does IgA cross epithelial cells?

A

Transcytosis

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116
Q

IgA caveat

A

Most produced antibody overall, but has lower serum concentrations.

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117
Q

What contains IgA

A

Tears, saliva, mucus, and breast milk.

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118
Q

What is secretory component?

A

Portion of IgA that IgA picks up from epithelial cells, and which protects Fc portion from luminal proteases.

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119
Q

What is produced in the immediate response to an antigen?

A

IgM

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120
Q

IgM forms

A

Monomer on B cell, pentamer with J chain when secreted.

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121
Q

Why does IgM exist as a pentamer?

A

Pentameric form enables avid binding to antigen while humoral response evolves.

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122
Q

IgD

A

Unclear function. Found on surface of many B cells and in serum.

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123
Q

What immunoglobulin has the lowest concentration in serum?

A

IgE

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124
Q

Thymus-independent antigens

A

Antigens lacking a peptide component. Thus, they can’t be presented by MHC to T cells and are weakly immunogenic.

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125
Q

Example of thymus-independent antigen

A

LPS

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126
Q

Critical function of CD40L

A

Class-switching. Expressed on helper T cells

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127
Q

What activates acute-phase reactants?

A

IL-6

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128
Q

What produces acute-phase reactants

A

liver

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129
Q

CRP function

A

Opsonin; fixes complement and facilitates phagocytosis

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130
Q

CRP clinical significance.

A

Sign of ONGOING inflammation.

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131
Q

Function of ferritin

A

Binds and sequesters iron to inhibit microbial iron scavenging.

132
Q

Functions of fibrinogen

A

1) coagulation factor
2) promotes endothelial repair
3) correlates with ESR.

133
Q

Function of hepcidin

A

1) decreases iron absorption (by degrading ferroportin)
2) decreased iron release (from macrophages)
*

134
Q

anemia of chronic disease mechanism

A

Increased hepcidin due to chronic inflammation.

135
Q

Serum amyloid A

A

acute phase reactant

136
Q

Transferrin mechanism

A

Internalized by macrophages to sequester iron.

137
Q

Why is albumin downregulated with inflammation?

A

Reduction conserves amino acids for positive reactants.

138
Q

MAC target

A

gram negative bacteria

139
Q

What activates classic complement pathway?

A

IgG or IgM

140
Q

What activates alternative complement pathway?

A

Microbe surface molecules

141
Q

What activates Lectin complement pathway?

A

Mannose or other sugars on microbe surface

142
Q

complement proteins involved in anaphylaxis

A

C3a, C4a, C5a

143
Q

MAC components

144
Q

C3b functions

A

1) opsonin

2) clears immune complexes

145
Q

Primary opsonins in bacterial defence

A

C3b and IgG

146
Q

What prevents complement activation of self cells?

A

1) decay-accelerating factor (DAF, aka CD55)

2) C1 esterase inhibitor

147
Q

C1 esterase inhibitor deficiency mechanism

A

unregulated activation of kallikrein leads to increased bradykinin

148
Q

DAF deficiency

A

Causes complement-mediated lysis of RBCs and PNH

149
Q

Other name for IL-1

A

Osteoclast-activating factor

150
Q

Il-1 functions

A

1) causes fever, acute inflammation
2) activates endothelium to express adhesion molecules
3) induces chemokine secretion to recruit WBCs

151
Q

IL-6 functions

A

1) fever

2) stimulates production of acute-phase proteins

152
Q

IL-12 functions

A

1) Induces differentiation of T cells into Th1 cells

2) activates NK cells

153
Q

TNF-alpha functions

A

1) sepsis
2) activates endothelium
3) causes WBC recruitment
4) vascular leak

154
Q

Cytokines secreted by macrophages

A

1,6,8,12,TNF-alpha

155
Q

cytokines secreted by all T cells

A

IL-2 and IL-3

156
Q

IL-2 functions

A

Stimulates growth of helper, cytotoxic, and regulatory T cells, and NK cells

157
Q

IL-3 functions

A
  • Supports growth and differentiation of bone marrow stem cells.
  • Functions like GM-CSF
158
Q

What secretes interferon-gamma

A

NK cells and Th1 cells in response to Il-12 from macrophages

159
Q

Interferon-gamma functions

A

1) stimulates macrophages to kill pathogens
2) inhibits differentiation of Th2 cells
3) activates NK cells to kill virus-infected cells.
4) Increases MHC expression and antigen presentation by all cells.

160
Q

cytokines secreted by Th2 cells

A

Il-4,5, and 10

161
Q

IL-4 functions

A

1) induces differentiation of T cells into Th2 cells
2) promotes growth of B cells
3) enhances class switching to IgE

162
Q

IL-5 functions

A

1) promotes growth and differentiation of B cells
2) enhances class switching to IgA
3) stimulates growth and differentiation of eosinophils

163
Q

IL-10 functions

A

1) attenuates inflammatory response
2) decreases expression of MHC class II and Th1 cytokines
3) inhibits activated macrophages and dendritic cells

164
Q

What is responsible for attenuating the immune response?

A

TGF-beta and IL-10

165
Q

NADPH functions

A

Creation AND neutralization of ROS.

166
Q

NADPH oxidase mechanism

A

Utilizes NADPH to generate oxygen anions

167
Q

Lactoferrin

A

Protein found in secretory fluids and neutrophils that inhibits microbial growth via iron chelation.

168
Q

Pyocyanin

A

enzyme in Pseudomonas that generates ROS to kill competing microbes

169
Q

Interferons

A

Glycoproteins synthesized by virus-infected cells that act locally on uninfected cells, priming them for viral defense by helping to selectively degrade viral nucleic acid and protein.

170
Q

Proteins found on T cells

A

1) TCR
2) CD3
3) CD28
4) CXCR4/CCR5

171
Q

CD3 function

A

Associated with TCR for signal transduction.

172
Q

CD28 function

A

Binds B7 on APC.

173
Q

Regulatory T cell markers

174
Q

B cell markers

A

1) Ig
2) CD19,20,21,40
3) MHC II
4) B7

175
Q

Ig function

A

Protein expressed on B cells that binds antigen.

176
Q

Proteins expressed on macrophages

A

1) CD14
2) CD40
3) CCR5
4) mHC II
5) B7 (CD80/86)
6) Fc and C3b receptors

177
Q

CD14 function

A

receptor for PAMPs

178
Q

NK cell markers

A

1) CD16

2) CD56 (unique marker for NK)

179
Q

CD16 on NK cells functions

A

Binds Fc of IgG

180
Q

Costimulatory signal

A

T and B cells need 2 signals to become activated. This is a safety mechanism of self-tolerance.

181
Q

Superantigen mechanism

A

Cross-link Beta region of T-cell receptor to MHC class II on APCs. Can activate any CD4+ T cell –> massive cytokine release.

182
Q

Endotoxins/LPS mechanism

A

Directly stimulate macrophages by binding to endotoxin receptor TLR4/CD14. No Th cells involved.

183
Q

bacterial examples of antigenic variation

A

1) salmonella
2) borrelia recurrentis
3) N gonorrhoeae

184
Q

viral examples of antigenic variation

A

1) influenza
2) HIV
3) HCV

185
Q

parisitic examples of antigenic variation

A

trypanosomes

186
Q

half-life of antibodies

187
Q

When are patients given preformed antibodies (which bugs?)?

A

“To Be Healed Very Rapidly”

Tetanus, Botulinium, HBV, Varicella, Rabies

188
Q

When are combined passive and active immunizations needed?

A

Hep B + rabies exposure

189
Q

Only live attenuated vaccine given to HIV patients

190
Q

Live attenuated vaccine mechanism

A

organism loses its pathogenicity but retains capacity for transient growth within inoculated host.

191
Q

Live attenuated vaccine pros/cons

A

Pro: induces strong, often lifelong immunity.
Con: can revert to virulent form.

192
Q

hep A vaccine: live or killed?

193
Q

polio (salk) vaccine: live or killed?

194
Q

BCG: vaccine: live or killed?

195
Q

varicella vaccine: live or killed?

196
Q

yellow fever vaccine: live or killed?

197
Q

measles vaccine: live or killed?

198
Q

Rabies vaccine: live or killed?

199
Q

influenza injection vaccine: live or killed?

200
Q

mumps vaccine: live or killed?

201
Q

rubella vaccine: live or killed?

202
Q

polio (sabin) vaccine: live or killed?

203
Q

site of action of histamine

A

postcapillary venules

204
Q

Type I hypersensitivity mechanism and delayed response.

A

1) Preformed antibodies on mast cells or basophil (IgE) are cross-linked with free antigens.
2) Delayed response follows due to production of archidonic acid metabolites (eg, leukotrienes).

205
Q

Type II mechanisms

A

1) opsonization and phagocytosis
2) Complement- and Fc receptor-mediated inflammation
3) Antibody-mediated cellular dysfunction

206
Q

Direct Coombs test

A

Detects antibodies that have adhered to patient’s RBCs (eg test Rh+ infant of an Rh- mother)

207
Q

Indirect coombs test

A

Detects serum antibodies that can adhered to other RBCs (test an Rh negative woman for Rh positive antibodies)

208
Q

Acute hemolytic transfusion reaction hypersensitivity type

209
Q

AIHA hypersensitivity type

210
Q

Type III hypersensitivity mechanism

A

Immune complexes activate complement, which attracts neutrophils; neutrophils release lysosomal enzymes.

211
Q

Polyarteritis nodosa hypersensitivity type

212
Q

Serum sickness mechanism

A

Antibodies to foreign proteins are produced. Immune complexes form and are deposited in membranes, where they fix complement, leading to tissue damage. Usually due to drugs acting as haptens.

213
Q

serum sickness presentation

A

Fever + urticaria + arthralgia + proteinuria + lymphadenopathy

214
Q

test for arthus reaction

A

immunofluorescent staining

215
Q

Arthus reaction mechanism

A

Local subacute antibody-mediated. Intradermal injection of antigen into presensitized (already has circulating IgG) individual leads to immune complex formation in skin.

216
Q

Arthus reaction presentation

A

edema + necrosis + complement activation.

217
Q

Type IV mechanism

A

1) Sensitized T cells encounter antigen and release cytokines, leading to macrophage activation.
2) Response does not involve antibodies.

218
Q

Type IV caveat

A

Not transferable by serum since cell mediated.

219
Q

Transplant rejections hypersensitivity type

220
Q

Febrile nonhemolytic transfusion reaction mechanism

A

Type II hypersensitivity reaction. Host antibodies against donor HLA antigens and WBCs

221
Q

Febrile nonhemolytic transfusion reaction presentation

A

Fever + headaches + chills + flushing

222
Q

Acute hemolytic transfusion reaction mechanism

A

Type II hypersensitivity reaction. Intravascular hemolysis (ABO blood group incompatibility) or extravascular hemolysis (host antibody reaction against foreign antigen on donor RBCs).

223
Q

Acute hemolytic transfusion reaction presentation

A

Fever + hypotension + tachypnea + tachycardia + flank pain + hemoglobinuria + jaundice (extravascular)

224
Q

hemoglobinuria

A

intravascular hemolysis

225
Q

Intravascular hemolysis

A

breakdown of RBCs in blood vessels

226
Q

extravascular hemolysis example

A

host antibody reaction against foreign antigen on donor RBCs

227
Q

drug-induced lupus antibody

A

anti-histone

228
Q

autoantibodies in polymyositis, dermatomyositis

A

Anti-Jo-1 + anti-SRP + anti-Mi-2

229
Q

primary membranous nephropathy autoantibody

A

antiphospholipase A2 receptor

230
Q

scleroderma autoantibody

A

Anti-Scl-70 (anti-DNA topoisomerase I)

231
Q

Autoimmune hepatitis type I autoantibody

A

anti-smooth muscle

232
Q

anti-SSA

233
Q

anti-SSB

234
Q

celiac disease autoantibodies

A

IgA anti-endomysial + IgA anti-tissue transglutaminase

235
Q

p-ANCA also known as

236
Q

c-ANCA also known as

237
Q

Other impt findings in bruton’s

A

Absenct/scanty lymph nodes and tonsils

238
Q

Bruton’s gene mutation

A

BTK (tyrosine kinase)

239
Q

Bruton’s presentation

A

Recurrent bacterial and enteroviral infections after 6 months (after maternal IgG declines).

240
Q

Most common primary immunodeficiency

A

Selective IgA deficiency

241
Q

CVD etiology

A

defect in B-cell differentiation

242
Q

term for cardiac defects in DiGeorge

A

Conotruncal abnormalities

243
Q

How do you test for 22q11 deletion?

244
Q

Immunodeficiency that prevents after adiminstration of BCG vaccine…

A

IL-12 receptor deficiency

245
Q

IL-12 receptor deficiency etiology

A

decreased Th1 response

246
Q

Labs in IL-12 receptor deficiency

A

decreased IFN-gamma

247
Q

hyper-IgE syndrome etiology

A

Deficiency of Th17 cells due to STAT3 mutation, leading to impaired recruitment of neutrophils to sites of infection.

248
Q

labs in hyper-IgE

A

Increased IgE + decreased IFN-gamma

249
Q

hyper-IgE presentation

A

Coarse facies, cold (noninflammed) staphylococcal abscesses, retained primary teeth, eczema.

250
Q

SCIDs etiology

A

either
1) Defective IL-2R gamma chain (x-linked)
OR
2) adenosine deaminase deficiency (AR)

251
Q

Findings in SCIDS

A

1) Decreased T-cell receptor excision circles (TRECs)
2) absence of thymic shadow on CXR
3) absence of germinal centers
4) absence T cells on flow cytometry.

252
Q

Findings in ataxia-telangiectasia

A

1) increased AFP
2) decreased IgA, IgG, and IgE
3) lymphopenia
4) cerebellar atrophy

253
Q

Hyper-IgM inheritance

A

X-linked recessive

254
Q

pathogens in Hyper-IgM

A

pneumocystis + cryptosporidium + CMV

255
Q

gene mutation in Wiskott-Aldrich syndrome

256
Q

Wiskott-Aldrich syndrome etiology

A

T cells unable to reorganize actin cytoskeleton.

257
Q

lab findings in Wiskott-ALdrich

A
  • decreased to normal IgG, IgM
  • Increased IgE, IgA
  • fewer and smaller platelets
258
Q

Wiskott-aldrich association

A

Increasedd risk of autoimmune disease and malignancy.

259
Q

Chediak-Higashi defect and etiology

A
  • Defect in lysosomal trafficking regulator gene (LYST).

- Microtubule dysfunction in phagosome-lysosome fusion.

260
Q

Chediak higashi presentation

A

1) Recurrent pyogenic infections by staphylococci and streptococci.
2) Partial albinism
3) peripheral neuropathy
4) progressive neurodegeneration
5) infiltrative lymphohistiocytosis.

261
Q

Findings in Chediak Higashi

A

1) Giant granules in granulocytes and platelets
2) pancytopenia
3) mild coagulation defects

262
Q

another name for flow cytometry

A

dihyrorhodamine test

263
Q

Catalase positive organisms

A 
Nocardia
Pseudomonas
Listeria
Aspergillus
Candida
E coli
Staphylococci
Serratia
B cepacia
H pylori
264
Q

Increased risk for… with deficiency in early complement

A

Encapsulated species.

265
Q

T cell deficiency leads to increased risk of…

266
Q

bacterial infections with decreased granulocytes (neutropenia)

A 
Staphylococcus
Burkholderia
Pseudomonas 
Serratia
Nocardia
267
Q

viral infections in B cell deficiency

A

Enteroviral encephalitis

Poliovirus (live vaccine contraindicated)

268
Q

Fungal infections in granulocyte deficiency (neutropenia)

A

Systemic candida

Aspergillus

269
Q

granulocytes

A

cells containing granules. Basophils, eosinophils, neutrophils.

270
Q

Syngeneic graft (isograft)

A

Graft from identical twin or clone

271
Q

Hyperacute graft rejection onset

A

within minutes

272
Q

Hyperacute graft rejection pathogenesis

A

Pre-existing recipient antibodies react to donor antigen, activating complement.

273
Q

Hyperacute graft rejection features

A

Widespread thrombosis of graft vessels –> ischemia/necrosis.

274
Q

Acute graft rejection timeframe

A

Weeks to months

275
Q

Acute graft rejection pathogenesis

A

Cellular: CD8+ T cells activated against donor MHcs (type IV
Humoral: similar to hyperacute, except antibodies develop after transplant.

276
Q

Acute graft rejection features

A

Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate

277
Q

Chronic graft rejection timeframe

A

Months to years

278
Q

Chronic graft rejection pathogenesis

A

CD4+ T cells respond to recipient APCs presenting donor peptides, including allogeneic MHC.
Both cellular and humoral components (type II and IV)

279
Q

Chronic graft rejection features

A

Recipient T cells react and secrete cytokines –> proliferation of vascular smooth muscle + parenchymal atrophy + interstitial fibrosis + ateriosclerosis.

280
Q

Lung chronic rejection disease

A

bronchiolitis obliterans

281
Q

heart chronic rejection disease

A

accelerated atherosclerosis

282
Q

kidney chronic rejection

A

chronic graft nephropathy

283
Q

liver chronic rejection disease

A

vanishing bile duct syndrome

284
Q

GVHD pathogenesis

A

Grafted immunocompetent T cells proliferate in immnocompromised host and reject host cells, leading to severe organ dysfunction.

285
Q

When does GVHD usually occur?

A

Bone marrow and liver transplants (rich in lymphocytes)

286
Q

When can GVHD be beneficial?

A

Potentially beneficial in bone marrow transplant for leukemia (graft-versus-tumor effect).

287
Q

Cyclosporine uses

A

1) transplant rejection prophylaxis
2) psoriasis
3) RA

288
Q

cyclosporine mechanism

A

Calcineurin inhibitors; binds CYCLOphilin.

Blocks T-cell activation by preventing IL-2 transcription.

289
Q

cyclosporine toxicity

A

nephrotoxic + HTN + hyperlipidemia + neurotoxicity + gingival hyperplasia + hirsitusm

290
Q

Tacrolimus MOA

A
  • Calcineuron inhibitor; binds FK506 binding protein FKBP.

- Blocks T-cell activation by preventing IL-2 transcription.

291
Q

Tacrolimus SE’s

A

Increased risk of diabetes + neurotoxicity + highly nephrotoxic.

292
Q

Sirolimus aka

293
Q

Sirolimus MOA

A

mTOR inhibitor; binds FKBP. Blocks T-cell activation and B-cell differentiation by preventing response to IL-2.

294
Q

Sirolimus toxicity

A

Pancytopenia + insulin resistance + hyperlipidemia.

295
Q

daclizumab, basiliximab SE’s

A

Edema + HTN + tremor

296
Q

Azathioprine MOA

A

antimetabolite precursor of 6-mercaptopurine.

- Inhibits lymphocyte proliferation by blocking nucletoide synthesis.

297
Q

Azathioprine uses

A

1) Transplant rejection prophylaxis
2) RA
3) Crohn’s
4) glomerulonephritis
5) other autoimmune conditions

298
Q

azathioprine SE’s

A

leukopenia + anemia + thrombocytopenia

299
Q

azathioprine contraindication

A

Allopurinol.

300
Q

Other use for mycophenolate mofetil

A

lupus nephritis

301
Q

mycophenolate mofetil association

A

Invasive CMV infection

302
Q

mycophenolate mofetil SE’s

A

GI upset + pancytopenia + HTN + hyperglycemia. Less nephrotoxic and neurotoxic.

303
Q

corticosteroid immunosuppression mechanism

A

1) Inhibit NF-kB.
2) Suppress both B- and T-cell function by decreasing transcription of many cytokines.
3) Induce apoptosis of T lymphocytes.

304
Q

Calcineurin action

A

NFAT-P–> NFAT, which is a TF

305
Q

aldesleukin

306
Q

aldesleukin clinical uses

A

RCC + metastatic melanoma

307
Q

Filgrastim

308
Q

Sargramostim

309
Q

IFN-alpha uses

A

Chronic hep B and C, Kaposi sarcoma, malignant melanoma

310
Q

Romiplostim, etrombopag

A

Thrombopoietin receptor agonists

311
Q

Oprelvekin

312
Q

alemtuzumab clinical use

313
Q

bevacizumab clinical uses

A

CRC + RCC + mac degen

314
Q

cetuximab target

315
Q

cetuximab uses

A

Stage IV CRC + head and neck cancer

316
Q

Rituximab target

317
Q

Rituximab uses

A

B-cell non-Hodgkin lymphoma + CLL + RA + ITP

318
Q

certolizumab target

A

soluble TNF-alpha

319
Q

etanercept MOA

A

decoy TNF-alpha receptor. NOT a monoclonal antibody.

320
Q

Eculizumab clinical use

A

Paroxysmal nocturnal hemoglobinuria

321
Q

Alpha4-integrin mechanism

A

WBC adhesion

322
Q

abciximab target

323
Q

denosumab mechanism

A

inhibits osteoclast maturation

324
Q

omalizumab target

325
Q

palivizumab target

A

RSV F protein

326
Q

monocytes

A

differentiate into macrophages, dendritic cells, and foam cells

STEP (85 decks)

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