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*First Aid in Brainscape* > Steve Irwin's Immunology Intellegence > Flashcards

Steve Irwin's Immunology Intellegence Flashcards

1
Q

Lymph nodes are

A

secondary lymphoid organs that have many afferents, 1 or more efferents. Encapsulated, with trabeculae. Functions are nonspecific filtration by macrophages, storage of B and T cells, and immune response activation. Functions are nonspecific filtration by macrophages, storage of B and T cells and immune response activation.

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2
Q

Follicle of a lymph node

A

Site of B cell localization and proliferation. In outer cortex. primary follicles are dense and dormant. secondary follicles have pale central germinal centers and are active

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3
Q

Medulla of lymph node

A

Consists of medullary cords (closely pack lymphocytes and plasma cells) and medullary sinuses. Medullary sinuses communicate with efferent lymphatics and contain reticular cells and macrophages.

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4
Q

Paracortex of lymph node

A

Houses T cells. Region of cortex between follicles and medulla. Contains high endothelial venules through which T and B cells enter from blood. Not well developed in patients with DiGeorge syndrome.

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5
Q

Cervical Lymph nodes drain what area of the body

A

Head and Neck

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6
Q

Hilar Lymph nodes drain what area of the body

A

Lungs

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7
Q

Mediastinal Lymph nodes drain what area of the body

A

Trachea and esophagus

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8
Q

Axillary Lymph nodes drain what area of the body

A

Upper limb, breast, skin above umbilicus

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9
Q

Celiac Lymph nodes drain what area of the body

A

Liver stomach spleen pancreas and upper duodenum

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10
Q

Superior mesenteric Lymph nodes drain what area of the body

A

Lower duodenum, jejunum, ileum, colon to splenic flexure

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11
Q

Inferior Mesenteric Lymph nodes drain what area of the body

A

Lower rectum to anal canal above the pectinate line, bladder, vagina (middle third), prostate

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12
Q

Para-aortic Lymph nodes drain what area of the body

A

Tests, ovaries, kidneys, uterus

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13
Q

Superficial inguinal Lymph nodes drain what area of the body

A

Anal canal (below pectinate line), skin below umbilicus (except popliteal territory)

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14
Q

Popliteal Lymph nodes drain what area of the body

A

Dorsolateral foot posterior calf

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15
Q

Right lymphatic duct drains what are

A

drains right side of body above diaphragm

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16
Q

Sinusoids of spleen

A

long, vascular channels in red pulp with fenestrated barrel hoop basement membrane. Macrophages found nearby

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17
Q

Where are T and B cells found in spleen

A

T cells: found in periarterial lymphatic sheath within the white pulp
B cells: found in follicles within the white pulp of the spleen.

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18
Q

What happens in the marginal zone of spleen

A

In between the red and white pulp: contains APCs and specialized B cells, where APCs present blood-borne antigens

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19
Q

Macrophages in the spleen do what?

A

Remove encapsulated spleen

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20
Q

Splenic dysfunction will lead to what

A

Decreased IgM leading to decreased complement causing decreased C3b opsonization and increased susceptibility to encapsulated organisms
Leads to infections form SHiNE SKiS:
Strep pneumoniae, H Influenza, Neisseria meningitidis, E coli, Salmonella, Klebsiella pneumoniae, group b Strep.

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21
Q

Thymus function:

A

Site of T cell differentiation and maturation. Encapsulated. from epithelium of 3rd pharyngeal pouch. Lymphocytes of mesenchymal origin. Cortex is dense with immature T cells; medulla is pale with mature T cells and Hassal corpuscles containing epithelial reticular cells.

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22
Q

Components of innate immunity

A

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

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23
Q

Components of adaptive immunity

A

T cells, B cells, circulating antibodies

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24
Q

What are the secreted proteins of innate immunity

A

lysozyme, complement, CRP, defensins

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25
Q

How does innate immune system recognize pathogen

A

Toll like receptors: pathogen recognition receptors that recognize pathogen-associated molecular patterns (PAMPs). Examples of PAMPs are LPS, flagellin, ssRNA

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26
Q

Gene loci of MHC I

A

HLA-A, HLA-B, HLA-C

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27
Q

Gene loci of MHC II

A

HLA-DR, HLA-DP, HLA-DQ

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28
Q

MHC I: binds

A

TCR and CD8

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29
Q

MHC II: binds

A

TCR and CD4

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30
Q

Function of MHC I

A

Present endogenously synthesized antigens (e.g. viral) to CD8+ cytotoxic T cells

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31
Q

Function of MHC II

A

Present exogenously synthesized proteins (e.g. bacterial proteins, viral capsid proteins) to T-Helper Cells

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32
Q

How is antigen loaded in MHC I

A

antigen peptides loaded onto MHC I in RER after delivery via TAP peptide transporter

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33
Q

How is antigen loaded in MHC II

A

Antigen loaded following release of invariant chain in an acidified endosome

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34
Q

HLA subtypes associated with: Hemochromatosis

A

A3

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35
Q

Diseases associated with B27 HLA

A

Psoriatic arthritis, Ankylosing spondylitis, arthritis of Inflammatory bowel disease, Reactive arthritis (PAIR)
This group of disorders is called seronegative arthropathies

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36
Q

HLA subtypes associated with: Celiac disease

A

DQ2/DQ8

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37
Q

Diseases associated with HLA DR2

A

Multiple sclerosis, hay fever, SLE, Goodpasture syndrome

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38
Q

Diseases associated with HLA DR3

A

Daibetes mellitus type 1, SLE, Graves disease

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39
Q

Diseases associated with HLA DR4

A

Rheumatoid arthritis, diabetes mellitus type 1

“there are 4 walls in a rheum”

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40
Q

Diseases associated with HLA DR5

A

pernicious anemia causing vitamin B12 deficiency, Hashimoto thyroiditis

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41
Q

Natural killer cells

A

Uses perforin and granzymes to induce apoptosis of virally infected cells and tumor cells. Only lymphocyte member of innate immune system.
Actively enhanced by IL-2, IL-12, IFN-beta, and IFN-alpha
induced to kill when exposed to a nonspecific activation signal on target cell and/or to an absence of MHC 1 on target cell surface.
Also kills via antibody-dependent cell-mediated cytotoxicity (CD16 binds Fc region of bound Ig, activating the NK cell).

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42
Q

Major functions of B cells

A

Recognize antigen-undergo somatic hypermutation to optimize antigen specificity. Produce antibody-differentiate into plasma cells to secrete specific immunoglobulins.
Maintain immunologic memory-memory b cells persist and accelerate future response to antigen

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43
Q

major functions of T cells

A

CD4+: help B cells make antibody and produce cytokines to activate other cells of immune system
CD8+: T cells kill virus infected cells directly. Delayed cell-mediated hypersensitivity (Type IV)
Acute and chronic cellular rejection
Rule of 8 “MHC 2 x CD4=8 and MHC 1 x 8=8”

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44
Q

Differentiation of T cells: Positive selection

A

happens in thymic cortex, T cells expressing TCRs capable of binding surface self MHC molecules survive

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45
Q

Differentiation of T cells: negative selection

A

Medulla. T cells expressing TCRs with high affinity for self antigens undergo apoptosis

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46
Q

How to get to a Th1 cell from a helper T cell

A

IL-12

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47
Q

how to get to a Th2 cell from a helper T cell

A

IL-4

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48
Q

How to get to a TH17 cell from a helper T cell

A

TGF-beta + IL-6

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49
Q

How to get to a Treg cell from a helper T cell

A

TGF-beta

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50
Q

Naive T cell activation

A
  1. foreign antigen is phagocytosed by dendritic cell
  2. foreign antigen is presented on MHC II and recognized by TCR on Th (helper) cell. Antigen is presented on MHC I to Tc (cytotoxic) cell.
  3. Costimulatory signal is given by interaction of B7 (on dendritic) and CD28 (on T cell)
  4. Th cell activates and produces cytokines. Tc cell activates and is able to recognize and kill virus infected cell
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51
Q

B cell activation and class switching

A
  1. helper T cell activation is completed
  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 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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52
Q

Th1 helper T cell: activated by? Activates? Inhibited by?

A

Secretes IFN-gamma
Activates macrophages and cytotoxic T lymphocytes (CD8)
Inhibited by IL-4 and IL-10 (from Th2 cells)

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53
Q

Th2 cells: activated by? Activates? inhibited by?

A

secretes IL-4, IL-5, IL-6, IL-13
Recruits eosinophils for parasite defense and promotes IgE production by B cells
Inhibited by IFN-gamma (from Th1 cells)

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54
Q

Macrophage-Lymphocyte interaction

A

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

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55
Q

Cytotoxic T cells

A

kill virus infected, neoplastic, and donor graft cells by inducing apoptosis.
Release cytotoxic granules containing preformed proteins (perforin-helps to deliver the content of granules into target cell, granzyme B- a serine protease, activates apoptosis inside target cells; granulysin-antimicrobial, induces apoptosis).
Cytotoxic T cells have CD8, which binds to MHC I on virus-infected cells

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56
Q

Regulatory T cells

A

Help maintain specific immune tolerance by suppressing CD4 and CD8 T cell effector function. Identified by expression of cell surface markers CD3, CD4, CD25 (alpha chain of IL-2 receptor), and transcription factor FOXP3
Activated regulatory T cells produce anti-inflammatory cytokines like IL-10 and TGF-beta

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57
Q

Fab region of antibody

A

Antigent-binding fragment

Determine idiotype: unique antigen binding pocket; only 1 antigenic specificity expressed per B cell

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58
Q

Fc region of antibody

A

Constant, Carboxy terminal, Complement binding, Carbohydrate side chains, Determines isotype (IgM, IgD….)`

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59
Q

Antibody diversity is generated by

A

Random Recombination of VJ (light chain) or V(D)J (heavy chain) genes
random combinations of heavy chains with light chains
Somatic hypermutation following antigen stimulation
Addition of nucleotides to DNA during recombination by terminal deoxynucelotidyl transferase

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60
Q

what part of antibody recognizes antigen

A

Variable part of the L and H chains

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61
Q

Fc portion of IgM and IgG fixes what

A

fixes complement

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62
Q

What do the heavy and light chains contribute to in the structure of an antibody

A

Heavy: both Fc and Fab fractions
Light: only Fab fraction

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63
Q

What do mature B lymphocytes express on their surface

A

IgM and IgD
(may differentiate in germinal centers of lymph nodes by isotype switching into plasma cells that secrete IgA, IgE, or IgG

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64
Q

IgG

A

main antibody in secondary (delayed) response to antigen. Most abundant isotype in serum. Fixes complement, crosses the placenta (provides infants with passive immunity), opsonizes bacteria, neutralizes bacterial toxins and viruses.

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65
Q

IgA

A

Prevents attachment of bacteria and viruses to mucous membranes; does not fix compliment
Monomer (in circulation) or Dimer (when secreted).
Crosses epithelial cells by transcytosis. Most produced antibody overall, but released into secretions (tears, saliva, mucus) and early breast milk (colostrum). Picks up secretory component from epithelial cells before secretions

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66
Q

IgM

A 
Produces in the primary (immediate) response to antigen
Fixes complement, does not cross placenta, Antigen receptor on the surface of B cells. Monomer on B cell or pentamer when secreted. Shape of pentamer allows it to efficiently trap free antigens out of tissue while humoral response evolves. #1 antibody if no class switching.
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67
Q

IgD

A

Unclear formation. found on the surface of many B cells and in serum

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68
Q

IgE

A

Bind mast cells and basophils; cross-links when exposed to allergen, mediating immediate (type-1) hypersensitivity through release of inflammatory mediators such as histamine. Mediates immunity to worms by activating eosinophils. Lowers concentration in serum.

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69
Q

Antigen type and memory: Thymus-independent antigens

A

Antigens lacking a peptide component (e.g. lipopolysaccharides form gram - bacteria); cannot be presented by MHC to T cells. Weakly or nonimmunogenic; vaccines often require boosters (e.g. pneumococcal polysaccharide vaccine). So major antibody will be IgM since no class switching

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70
Q

Antigen type and memory: thymus dependent antigens

A

Antigens containing a protein component (e.g. diptheria vaccine). Class switching and immunologic memory occur as a result of direct contact of B cells with Th cells (CD40-CD40 ligand reaction).

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71
Q

What are acute phase reactants

A

Factors whose serum concentrations change significantly in response to inflammation; produced by the liver in both acute and chronic inflammatory states. Induced by IL-1, 6, TNF alpha, and IFN-gamma

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72
Q

Acute Phase reactant: Serum amyloid A

A

Upregulated: prolonged elevation can lead to amyloidosis

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73
Q

Acute Phase reactant: C reactive protein

A

Upregulated: opsonin that fixes complement and facilitates phagocytosis

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74
Q

Acute Phase reactant: Ferritin

A

Upregulated: Binds and sequesters iron to inhibit microbial scavenging

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75
Q

Acute Phase reactant: Fibrinogen

A

Upregulated: Coagulation factor; promotes endothelial repair; correlates with ESR

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76
Q

Acute Phase reactant: Hepcidin

A

upregulated: Prevents release of iron bound by ferritin can lead to anemia of chronic disease

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77
Q

Acute Phase reactant: albumin

A

downregulated: reduction conserves amino acids for positive reactants

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78
Q

Acute Phase reactant: Transferrin

A

Downregulated: internalized by macrophages to sequester iron

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79
Q

Membrane Attack Complex (MAC) defends against what type of bacteria

A

Gram negative bacteria

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80
Q

Name the three complement pathways

A

Classic, Alternative and Lectin

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81
Q

How do you activate the different complement pathways

A

Classic: IgG or IgM mediated
Alternative pathway: microbe surface molecules
Lectin pathway: mannose or other sugars on microbe surface

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82
Q

What does this complement component do: C3b

A

opsonization, helps clear immune complexes

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83
Q

What does this complement component do: C3a

A

anaphylaxis

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84
Q

What does this complement component do: C4a

A

anaphylaxis

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85
Q

What does this complement component do: C5a

A

anaphylaxis and neutrophil chemotaxis

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86
Q

What does this complement component do: C5b-9

A

cytolysis by membrane attack complex

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87
Q

How do you inhibit complement system

A

Decay-accelerating factor (DAF, aka CD55) and C1 esterase inhibitor help prevent complement activation on self cells (e.g. RBC)

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88
Q

What is the C3 convertase for the alternative pathway

A

C3bBb

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89
Q

What is the C3 convertase for the lectin pathway

A

C4b2b

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90
Q

What is the C3 convertase for the classic pathway

A

C4b2b

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91
Q

What is the C5 convertase for the alternative pathway

A

C3bBb3b

92
Q

What is the C5 convertase for the lectin pathway

A

C4b2b3b

93
Q

What is the C5 convertase for the Classic pathway

A

C4b2b3b

94
Q

C1 esterase inhibitor deficiency

A

Causes hereditary angioedema. ACE inhibitors are contraindicated

95
Q

C3 deficiency

A

Increases risk for severe, recurrent pyogenic sinus and respiratory infections; increase susceptibility to type III hypersensitivity reactions

96
Q

C5-C9 deficiency

A

Increase susceptibility to recurrent Neisseria bacteremia

97
Q

DAF (GPI anchored enzyme) deficiency

A

Causes complement-mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria

98
Q

IL-1

A

secreted from macrophages
An endogenous pyrogen also called osteoclast-activating factor
Causes fever, acute inflammation. Activates endothelium to express adhesion molecules; induces endothelium to express adhesion molecules; induces chemokine secretion to recruit leukocytes.

99
Q

IL-6

A

secreted by macrophages and Th2 cells
an endogenous pyrogen
causes fever and stimulates production of acute-phase proteins

100
Q

IL-8

A

Secreted by macrophages

Major chemotactic factor for neutrophils.

101
Q

IL-12

A

secreted by macrophages

induces differentiation of T cells into Th1 cells. Activates NK cells. Also secreted by B cells

102
Q

TNF-alpha

A

secreted by macrophages

Mediates septic shock. Activates endothelium. Causes leukocyte recruitment, vascular leak

103
Q

IL-2

A

Secreted by all T cells

Stimulates Growth of helper, cytotoxic and regulatory T cells

104
Q

IL-3

A

Secreted by all T cells

Supports the growth and differentiation of bone marrow stem cells. Functions like GM-CSF

105
Q

Interferon-gamma

A

Secreted from Th1 cells
Has antiviral and anti-tumor properties. Activates NK cells to kill virus-infected cells, Increases MHC expression and antigen presentation in all cells

106
Q

IL-4

A 
Secreted from Th2 cells
Induces differentiation into Th2 cells. Promotes growth of B cells. Enhances class switching to IgE and IgG
107
Q

IL-5

A 
Secreted from Th2 cells
Promotes differentiation of B cells. Enhances class switching to IgA. Stimulates the Growth and differentiation of eosinophils.
108
Q

IL-10

A

Secreted form Th2 cells and regulatory T cells
Modulates inflammation response. Inhibits actions of activated T cells and Th1.
TGF-Beta has similar actions to IL-10 because it it involved in inhibiting inflammation

109
Q

Cytokines secreted by macrophages

A

IL-1, IL-6, IL-8, IL-12, INF alpha

110
Q

Cytokines secreted by all T cells

A

IL-2, IL-3

111
Q

Cytokines secreted by Th1 cells

A

IL-2, IL-3 (all t cells)

Interferon-gamma

112
Q

Cytokines secreted by Th2 cells

A

IL-2, IL-3 (all t cells)

IL-4, IL-5, IL-10

113
Q

Interferon alpha and Beta

A

Interferes with viruses
A part of innate host defense against both RNA and DNA viruses. Interferons are glycoproteins synthesized by viral-infected cells that act locally on uninfected cells, “priming” them for viral defense. When a virus infects “primed” cells, viral dsRNA activates: RNAase L (degrades viral/host mRNA) and Protein kinase (inhibition of viral/host protein synthesis)
Essentially results in apoptosis, thereby interrupting viral amplifications

114
Q

Cell surface protein: T cells

A

TCR (binds antigen-MHC complex)
CD3 (associated with TCR for signal transduction)
CD28 (binds B7 on APC)

115
Q

Cell surface protein: Helper T cells

A

CD4 and CD40 ligand

116
Q

Cell surface protein: cytotoxic T cells

A

CD8

117
Q

Cell surface protein: B cells

A

Ig (binds antigen)
CD-19, CD 20, CD21 (receptor for EBV), CD40
MHC II, B7
(has CD5 when premature, if mature and has CD5 then they have Chronic lymphocytic leukemia)

118
Q

Cell surface proteins on Macrophages

A

CD14, CD40
MHC II, B7
Fc and C3b receptors (enhanced phagocytosis)

119
Q

Cell surface proteins on NK cells

A

CD16 (binds Fc of IgG), CD56 (unique marker for NK)

120
Q

Anergy

A

Self-reactive T cells become nonreactive without co-stimulatory molecule. B cells also become anergic, but tolerance is less complete than in T cells

121
Q

Effects of bacterial toxins: Superantigens (pyogenes and aureus)-

A

cross-link Beta region of the T cell receptor to the MHC class II on APCs. Can activate any t cell, leading to massive release of cytokines.

122
Q

Effects of bacterial toxins: endotoxins/lipopolysaccharide (gram negative bacteria):

A

stimulate macrophages by binding to endotoxin receptor CD14; Th cells are not involved

123
Q

Passive immunity

A

Receive preformed antibodies
Rapid Onset
Short span of antibodies (3 week half life)
Examples: IgA in breast milk, maternal IgG crossing placenta, antitoxin (Tetanus, botulinum, HBV, Rabies), humanized monoclonal antibody

124
Q

Active immunity

A

Exposure to foreign antigens gives you the immunity
Slow onset
Long-lasting protection
Examples would be natural infection, vaccines, toxoid

125
Q

Combine active and passive immunizations are given after exposure to what diseases

A

Hepatitis B and Rabies

126
Q

Vaccinations cause:

A

Autism

Source: jennymaccarthy_antivax_naturopathy@blogspot.com

127
Q

Live attenuated viruses

A

Microorganism loses its pathogenicity but retains capacity for transient growth within inoculated host. Mainly induces a cellular response.
Induces strong often lifelong immunity
May revert to virulent form and often contraindicated in pregnancy and immune deficiency
Examples: MMR, Sabin polio, intranasal influenza, varicella, yellow fever

128
Q

Inactivated virus or killed virus vaccines

A

Pathogen in inactivated by heat or chemicals; maintaining epitope structure on surface antigens is important for immune response. Humoral immunity induced.
Stable and safer than live vaccines
Weaker immunity response; booster shots usually required
Examples: Cholera, Hepatitis A, Polio (salk), influenza injection form, rabies

129
Q

Type 1 hypersensitivity

A 
Anaphylactic and atopic- free antigen cross links IgE on presensitized mast cells and basophils, triggering immediate release of vasoactive amines that act at postcapillary venules (i.e. histamine). Reaction develops rapidly after antigen exposure because of preformed antibody. Delayed response follows due to production of arachidonic acid metabolites (e.g. leukotrienes)
Get urticaria (hives)
Tests: skin test for specific IgE
130
Q

Type 2 Hypersensitivity

A

Cytotoxic (antibody mediated) IgM, IgG bind to fixed antigen on “enemy” cell, leading to cellular destruction.
3 Mechanisms: 1. Opsonization leading to phagocytosis or complement activation 2. Complement-mediated lysis 3. Antibody dependent cell-mediated cytotoxicity, usually due to NK cells or macrophages.
Type II is cy-2-toxic
Antibody + complement leads to MAC
Test: direct and indirect Coombs’

131
Q

Direct Coombs’

A

Detect antibodies that have adhered to patient’s RBCs (e.g. test an RH + infant of an Rh - mother)

132
Q

Indirect Coombs’

A

Detects antibodies that can adhere to other RBCs (e.g. test an Rh- woman for Rh+ antibodies)

133
Q

Type III hypersensitivity

A

Immune complex- antigen antibody (IgG) complexes activate complement, which attracts neutrophils; neutrophils release lysosomal enzymes
Type 3=3 things get stuck together= antigen-antibody-complement

134
Q

Serum sickness

A

An immune complex disease (type 3) in which antibodies to foreign proteins are produced (takes 5 days). Immune complexes form and are deposited in membranes, where the fix complement (leads to tissue damage). More common that Arthus reaction
Most serum sicknesses are now caused by drugs (not serum) acting as haptens. Fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days after antigen exposure.

135
Q

Arthus reaction

A

a local subacute antibody mediated hypersensitivity (type 3) reaction. Intradermal injection of antigen induces antibodies, which form antigen-antibody complexes in the skin. Characterized by edema, necrosis, and activation of complement
Antigen-antibody complexes cause the Arthus reaction
Test: immunofluorescent staining
(e.g. tetanus booster causing swelling in arm, you already have pre formed antibodies which react with antigen)

136
Q

Type IV hypersensitivity

A

Delayed (t cell mediated) type- sensitized T lymphocytes encounter antigen and then release lymphokines (leads to macrophage activation; no antibody involved)
Cell mediated=not transferable by serum
4T’s= T lymphocytes, Transplant rejections, Tb skin test, Touching (contact dermatitis).

137
Q

Blood transfusion reactions: allergic reaction

A

Type 1 hypersensitivity reaction against plasma proteins in transfused blood.
Get Urticaria, pruritus, wheezing, fever.
Treat with antihistamines

138
Q

Blood transfusion reactions: anaphylactic reaction

A

severe allergic reaction. IgA-deficient individuals must receive blood products that lack IgA
Get dyspnea, bronchospasm, hypotension, respiratory arrest, shock.

139
Q

Blood transfusion reactions: Febrile nonhemolytic transfusion reaction

A

Type II hypersensitivity reaction. Host antibodies against HLA antigens and leukocytes
Get Fever, Headaches, chills, flushing

140
Q

Blood transfusion reactions: Acute Hemolytic transfusion reaction

A

Type II hypersensitivity reaction. Intravascular hemolysis (ABO blood group incompatibility) or extravascular hemolysis (host antibody reaction against foreign antigen on donor RBCs).
Get fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinemia (intravascular), jaundice (extravascular hemolysis)

141
Q

What disease is associated with this auto-antibody: Anti-ACh

A

Myasthenia gravis

142
Q

What disease is associated with this auto-antibody: anti-basement membrane

A

Goodpasture Syndrome

143
Q

What disease is associated with this auto-antibody: anti-cardiopilin

A

SLE

144
Q

What disease is associated with this auto-antibody: anticentromere

A

Limited scleroderma (CREST)

145
Q

What disease is associated with this auto-antibody: anti-desmoglein

A

Pemphigus vulgaris

146
Q

What disease is associated with this auto-antibody: anti-dsDNA, anti-Smith

A

SLE

147
Q

What disease is associated with this auto-antibody: Anti-glutamate decarboxylase

A

Type 1 diabetes

148
Q

What disease is associated with this auto-antibody: anti-hemidesmosome

A

bullous pemphigoid

149
Q

What disease is associated with this auto-antibody: Antihistone

A

Drug-induced lupus

150
Q

What disease is associated with this auto-antibody: anti-Jo-1, anti SRP, Anti-mi-2

A

Polymyositis, Dermatomyositis

151
Q

What disease is associated with this auto-antibody: Antimicrosomal, antithyroglobulin

A

Hoshimoto thyroiditis

152
Q

What disease is associated with this auto-antibody: Antimitochondrial

A

Primary Biliary cirrhosis

153
Q

What disease is associated with this auto-antibody: antinuclear antibodies

A

SLE, nonspecific

154
Q

What disease is associated with this auto-antibody: Anti-Scl-70 (anti-DNA topoisomerase I)

A

Scleroderma (diffuse)

155
Q

What disease is associated with this auto-antibody: anti-smooth muscle

A

Autoimmune hepatitis

156
Q

What disease is associated with this auto-antibody: Anti-SSA, anti-SSB (anti-Ro, anti-La)

A

Sjorgen syndrome

157
Q

What disease is associated with this auto-antibody: Anti-TSH

A

Graves disease

158
Q

What disease is associated with this auto-antibody: Anti-U1 RNP (ribonucleoprotein)

A

Mixed connective tissue

159
Q

What disease is associated with this auto-antibody: c-ANCA (PR3-ANCA)

A

Granulomatosis with polyangiitis (Wegener)

160
Q

What disease is associated with this auto-antibody: IgA anti-endomysial, IgA anti-tissue transglutaminase

A

Celiac disease

161
Q

What disease is associated with this auto-antibody: p-ANCA (MPO-ANCA)

A

Microscopic polyangitis, Churg-Strauss Syndrome

162
Q

What disease is associated with this auto-antibody: Rheumatoid factor (antibody, most commonly IgM, specific to IgG Fc region), anti-CCP

A

Rheumatoid arthritis

163
Q

What bacteria are bad if you have no B cells

A

Fine unless you get SHiNE SKiS

Strep pneumoniae, H influenza type b, Neisseria meningitidis, E coli, Salmonella, Klebsiella pneumoniae, group b Strep

164
Q

What bacteria are bad if you have no granulocytes

A

fine unless you get, staphylococcus, Burkholderia cepacia, Serratia, Nocardia
Then you cannot fight it off

165
Q

What bacteria are bad if you have no complement

A

Be fine, unless you get Neisseria (no MAC)

166
Q

If you have no T cells what viral infection should you stay away from

A

CMV, EBV, JCV, VZV, Chronic infection with respiratory/GI viruses

167
Q

If you have no B cells, what Viruses are really bad

A

Enteroviral encephalitis, poliovirus

And do not give live vaccine

168
Q

If you have no T cells, what fungi are really bad

A

Candida, PCP (not the drug! Pneumocystis pneumonia)

169
Q

If you have no granulocytes, what fungi are really bad

A

Candida, Aspergillus

170
Q

Immunodeficiencies: Compare T cell VS B cell deficiency

A

T cell deficiency: tend to produce more recurrent fungal and viral infections
B cell deficiency: tend to produce more recurrent bacterial infections

171
Q

X-linked (Bruton) agammaglobulinemia

A

Defect in BTK, a tyrosine kinase gene leading to no B cell maturation. X-linked recessive
Presents: recurrent bacterial and enteroviral infections after 6 months (lose maternal IgG)
Findings: normal CD19+ B cell count, decrease pro-B, decrease Ig of all classes. Absent/scanty lymph nodes and tonsils

172
Q

Selective IgA deficiency

A

unknown. most common primary immunodeficiency. decreased IgA=> increase class switching to IgE=> more atopy (allergies)
Presentation: Majority asymptomatic, can see airway and GI infections, Autoimmune disease, Atopy, Anaphylaxis to IgA containing products.
Findings: decreased plasma cells, decreased immunoglobulins

173
Q

Common variable immunodeficiency

A

Defect in B cell differentiation. Many causes
Presentation: can be acquired in 20s and 30s; increased risk of autoimmune disease, bronchiectasis, lymphoma, sinopulmonary infections.
Findings: decrease plasma cells, decrease immunoglobulins, can still have intact cellular immunity (e.g. will respond to candida skin test)

174
Q

Thymic aplasia (Digeorge syndrome)

A

22q11 deletion; failure of 3rd and 4th pharyngeal pouches to develop leading to absent thymus and parathyroids.
Presentation: Tetany (hypocalcemia), recurrent viral/fungal infections (T-cell deficiency), conotruncal abnormalities (e.g. tetrology of Fallot, Truncus arteriosus).
Findings: decreased T cells, decreased PTH, decreased Calcium. Abscent thymic shadow on CXR, 22q11 deletion seen on FISH

175
Q

IL-12 receptor deficiency

A

Decreased Th1 response. Autosomal recessive
Presentation: Disseminated mycobacterial and fungal infections; may present after administration of BCG (TB) vaccine.
Findings: decreased IFN-gamma

176
Q

Autosomal dominant hyper-IgE syndrome (Job Syndrome)

A

Deficiency of Th17 cells due to STAT3 mutation leading to impaired recruitment of neutrophils to sites of infection
Presentation: FATED; coarse Facies, cold (noninflamed) staphylococcal Abscesses, retained primary Teeth, increased igE, Dermatologic problems (eczema)
Findings: Increased IgE and decreased IFN-gamma

177
Q

Chronic Mucocutaneous candidiasis

A

T-cell dysfunction. Many causes
Presentation: Noninvasive Candida albicans infections of skin and mucous membranes.
Findings: Absent in vitro T-cell proliferation in response to Candida antigens. Absent cutaneous reaction to Candida antigens.

178
Q

Severe combined immunodeficiency (SCID)

A

Several types including defective IL-2R gamma chain (most common, X linked), adenosine deaminase deficiency (autosomal recessive).
Presentation: failure to thrive, chronic diarrhea, thrush. Recurrent viral, bacterial, fungal, and protozoal infections.
Treatment: bone marrow transplant (no concern for rejection)
Findings: T cell receptor excision circles (TRECs); Absence of thymic shadow (CXR), germinal centers (lymph node biopsy), and T cells (flow cytometry)

179
Q

Ataxia-telangiectasia

A

Defects in ATM gene leading to DNA double stranded breaks causing cell cycle arrest
Presentation: cerebellar defects (ataxia), spider angiomas (telangiectasia of eyes and skin), IgA deficiency, increased change of Hodgkins and lymphomas
Findings: Increased AFP; decreased IgA, IgG and IgE; lymphopenia, cerebellar atrophy;
autosomal recessive

180
Q

Hyper-IgM syndrome

A

Most commonly due to defective CD40L on Th cells=class switching defect; X linked recessive
Presentation: Severe pyogenic infections early in life; opportunistic infection with Pneumocystis, Cryptosporidium, CMV
Findings: Increased IgM; Greatly decreased IgG, IgA, IgE

181
Q

Wiskott-Aldrich syndrome

A

Mutation in WAS gene (x-linked recessive); T cells unable to reorganize actin cytoskeleton.
Presentation (WATER): Wiskott-Aldrich, Thrombocytopenic purpura, Eczema, Recurrent infections; increased risk of autoimmune diseases and non hodgkin lymphoma

182
Q

Leukocyte adhesion deficiency Type 1

A

Defect in LFA-1 integrin (CD18) protein on phagocytes; impaired migration and chemotaxis; autosomal recessive.
Recurrent bacterial skin and mucosal infections, absent pus formation, impaired wound healing, delayed separation of umbilical cord (>30 days).
Findings: increased neutrophils, absence of neutrophils at infection sites

183
Q

Chediak-Higashi syndrome

A

Defect in lysosomal trafficking regulator gene (LYST); microtubule dysfunction in phagosome-lysosome fusion; autosomal recessive
Presentation: Recurrent pyogenic infections by staph and strep, partial albinism, peripheral neuropathy, progressive neurodegeneration, infiltrative lymphohistiocytosis.
Findings: increased neutrophils, absence of neutrophils at infection site

184
Q

Chronic granulomatous disease

A

Defect of NADPH oxidase leading to a decrease in reactive oxygen species (e.g. superoxide) and absent respiratory burst in neutrophils; X linked recessive
Presentation: increased susceptibility to catalase positive organisms (PLACESS): Pseudomonas, Listeria, Aspergillus, Candidia, E coli, S. aureus, Serratia
Findings: abnormal dihydrorhodamine (flow cytometry) test. Nitroblue tetrazolium dye reduction test is negative (test out of favor now)

185
Q

What is an autograft

A

graft from self to self

186
Q

What is a syngeneic graft

A

from identical twin or clone (because clones are thing…..)

187
Q

what is an Allograft

A

From nonidentical individual of same species

188
Q

what is a Xenograft

A

a graft from a different species

189
Q

Transplant rejection: Hyperacute

A

occurs within minutes
Pathogenesis: pre-existing antibodies react to donor antigen (type II reaction), activate complement.
Features: widespread thrombosis of graft vessels leading to ischemia/necrosis. Graft must be removed.

190
Q

Transplant rejection: Acute

A

occurs in weeks to months
Pathogenesis: Cellular: CTLs activated against donor MHCs. Humoral: similiar to hyperacute but antibodies develop after transplant
Features: Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate. Prevent/reverse with immunosuppressants

191
Q

Transplant rejection: Chronic

A

occurs in Months to years
Pathogenesis: Recipient T cells perceive donor MHC as recipient MHC and react against donor antigens present. Both cellular and humoral components
Features: irreversible, T cell and antibody mediated damage. Organ specific: Heart-atherosclerosis, Lungs-bronchiolitis obliterans, Liver-Vanishing bile ducts, Kidney-vascular fibrosis and glomerulopathy

192
Q

Transplant rejection: Graft-Versus-host disease

A

Onset varies
Pathogenesis: grafted immunocompetent T cells proliferate in the immunocompromised host and reject host cells with “foreign” proteins leading to severe organ dysfunction.
Features: Maculopapular rash, jaundice, diarrhea, hepatosplenomegaly, Usually in bone marrow and liver transplants (high in lymphocytes). Potentially beneficial in bone marrow transplant for leukemia (graft-versus-tumor effect)

193
Q

Cyclosporine

A

Mechanism: calcineurin inhibitor; binds cyclophilin; blocks t cell activation by preventing IL-2 transcription
Uses: transplant rejection prophylaxis, psoriasis, rheumatoid arthritis
Toxicity: !Nephrotoxicity!: hypertension, hyperlipidemia, hyperglycemia, tremor, hirsutism, gingival hyperplasia (all of the hypers)

194
Q

Tacrolimus

A

Calcineurin inhibitor; binds FK506 binding protein (FKBP) (all -limus drugs bind FKBP). Blocks T cell activation by preventing IL-2 transcription.
Uses. Transplant rejection prophylaxis
Toxicity: similar to cyclosporine (nephrotoxic), increase risk of diabetes and neurotoxicity; no gingival hyperplasia or hirsutism.

195
Q

Sirolimus (Rapamycin)

A

mTOR inhibitor; binds FKBP. Blocks T cell activation and B cell differentiation by preventing IL-2 transduction.
Uses: Kidney transplant rejection prophylaxis
Toxicity: anemia, thrombocytopenia, leukopenia, insulin resistance, hyperlipidemia; non-nephrotoxic.
Notes: Kidney “sir-vives.” Synergistic with cyclosporine. Also used in drug eluting stents.

196
Q

Basiliximab

A

Monoclonal antibody; blocks IL-2R
Uses: kidney transplant rejection prophylaxis.
Toxicity: edema, hypertension, Tremor

197
Q

Azathioprine

A

antimetabolite precursor for 6-mercaptopurine; inhibits lymphocyte proliferation by blocking nucleotide synthesis.
Uses: Transplant rejection prophylaxis, rheumatoid arthritis, Crohn disease, Glomerulonephritis, other autoimmune conditions
Toxicity: Leukopenia, anemia, thrombocytopenia
Note: 6-MP is degraded by xanthine oxidase so toxicity is increased by allopurinol

198
Q

Glucocorticoids

A

Inhibit NF-kappaB. Suppress both B and T cell function by decreasing transcription of many cytokines.
Uses: transplant rejection prophylaxis (immune suppression), many autoimmune disorders, inflammation.
Toxicity: hyperglycemia, osteoporosis, central obesity, muscle breakdown, psychosis, acne, hypertension, cataracts, peptic ulcers.
Can cause iatrogenic Cushing syndrome

199
Q

Recombinant cytokines and their clinical uses: Epoetin alfa

A 
erythropoietin
Treats anemias (Especially in renal failure)
200
Q

Recombinant cytokines and their clinical uses: Thrombopoietin

A

Treats thrombocytopenia

201
Q

Recombinant cytokines and their clinical uses: Oprelvekin

A

(IL-11) Treats thrombocytopenia

202
Q

Recombinant cytokines and their clinical uses: Filgrastim

A

granulocyte colony-stimulating factor

Used for recovery of bone marrow

203
Q

Recombinant cytokines and their clinical uses: Sargramostim

A

Granulocyte-macrophage colony-stimulating factor)

used for the recovery of bone marrow

204
Q

Recombinant cytokines and their clinical uses: Aldesleukin

A

IL-2

Used for Renal cell carcinoma, metastatic melanoma

205
Q

Recombinant cytokines and their clinical uses: IFN-alpha

A

used for Chronic hep B and C, Kaposi sarcoma, Hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma

206
Q

Recombinant cytokines and their clinical uses: IFN-beta

A

Used for multiple sclerosis

207
Q

Recombinant cytokines and their clinical uses: IFN-gamma

A

Used for chronic granulomatous disease

208
Q

Target and use for: alemtuzumab

A

targets CD52
used for CLL
aLYMtuzumab for chronic LYMphocytic leukemia

209
Q

Target and use for: Bevacizumab

A

target is VEGF

used for: colorectal cancer, renal cell carcinoma

210
Q

Target and use for: Cetuximab

A

target is EGFR

used for Stage IV colorectal cancer, head and neck cancer

211
Q

Target and use for: Rituximab

A

target is CD20

Clinical use is B cell non hodgkin lymphoma, rheumatoid arthritis (with MTX), ITP

212
Q

Target and use for: Trastuzumab

A

Target is HER2/neu
Used for breast cancer, gastric cancer
“HER2-tras2zumab

213
Q

Target and use for: Inflizimab, adaliumab

A

Target is TNF-alpha
used for IBD, rheumatoid arthritis, ankylosing spondylitis, psoriasis
Rheumatoid arthritis “infilx” pain in “da limbs”

214
Q

Target and use for: Natalizumab

A

Target is alpha 4 integrin
Used for Multiple sclerosis, Crohn disease
Notes: alpha 4 integrin is for leukocyte adhesion, also get risk of PML in patients with JC virus

215
Q

Target and use for: Abciximab

A

Targets Glycoprotein IIb/IIIa
Used as an anti-platelet agent for prevention of ischemic complications in patients undergoing percutaneous coronary intervention
IIb times IIIa equals abSIXimab

216
Q

Target and use for: Denosumab

A

Target is RANKL
Used for Osteoporosis; inhibits osteoclast maturation (mimics osteoprotegrin)
Notes: denOSumab affects OSteoclasts

217
Q

Target and use for: Digoxin immune Fab

A

Target: digoxin

Used as the antidote for digoxin toxicity

218
Q

Target and use for: Omalizumab

A

Target is IgE

Used for allergic asthma; prevents IgI binding to FceRI

219
Q

Target and use for: Palivizumab

A

Targets RSV F protein
used for: RSV prophylaxis for high-risk infants
Notes: paliVIzumab for VIruses

220
Q

Which complement pathway will clear antigen-antibody complexes (type 3 hypersensitivity)

A

Classical because it has C3 which clears complexes and classic pathway is activated by IgM and IgG (alternative pathway is not activated by IgM and IgG)

221
Q

Microctotoxicity test:

A

Determines if donor and recipient have matching HLA-A, B, and C (MHC class I), prevents against immune response

222
Q

A CD19+ cell is what type

A

it is a B cell

223
Q

A CD 14+ cell is what type

A

macrophage

224
Q

What do you use to do a paternity test?

A

Use allotypes from immunoglobulins. They show distinct patterns of inheritance but do not affect the action of the immunoglobulins

225
Q

B cell is identified by what CD markers

A

CD 19, 20, 21

226
Q

CD55 identifies

A

complement decay-accelerating factor: is on all hemopoietic and non hemopoietic cells: blocks MAC: low levels or absence leads to paroxysmal nocturnal hemoglobinuria

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