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Immunology > Prep For Exam > Flashcards

Prep For Exam Flashcards

1
Q

Define: PAMPs

A

Recognized by innate immune system; Shared characteristics of many pathogens (including LPS, CpG DNA, mannose, flagellum, dsRNA)

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2
Q

What does the complement system do?

A

Lyses the pathogen cell; opsonizes pathogen; recruits phagocytes

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3
Q

What are the 3 types of phagocytes?

A

Macrophages; neutrophils; dendritic cells

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4
Q

What are the components of the innate immune system?

A

Complement cascade; phagocytes; natural killers

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5
Q

Where do T cells develop?

A

They are derived from pluripotent stem cells that are located in the bone marrow and then they develop in the thymus

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6
Q

How long does T cell development take?

A

3 weeks

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7
Q

What are the parts of the thymus?

A

Peripheral cortex (densely populated w/ lymphoid cells) and central medulla (less lymphocyte rich, contains DCs and macrophages)

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8
Q

What are the 3 stages of T cell development?

A 
Double negative (CD4-/8-); double positive (CD4+/8+); single positive (express CD4 or CD8 only)
NOTE: DN thymocytes are not committed to T cell lineage (can become B or NK cells)
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9
Q

Define: Alpha Beta T Cells

A

Surface TCR composed of alpha and beta chains; most abundant; responsible for adaptive immune response

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10
Q

Define: Gamma-delta T Cells

A

Surface TCR composed of gamma and delta T cells; minor population; recognizes lipid antigens in the gut

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11
Q

How do T cells decide whether they should become gamma-delta or alpha-beta?

A

DN T cells rearrange their beta, gamma, and delta; if beta chain successfully rearranges, then it becomes a pre-TCR; if gamma and delta chains rearrange, then they commit to gamma-delta lineage; NOTCH signaling can also influence choice

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12
Q

How many rounds of recombination does TCRbeta chain go through?

A

2, due to the two D-J clusters and C domains;
If unsuccessful, then the cell dies;
If successful, then the TCRbeta is expressed with pre-TCRalpha on the cell surface

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13
Q

What do B cells in the mucosa express?

A

IgA

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14
Q

What makes a pentameter?

A

IgM

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15
Q

What segments does the light chain have? The heavy?

A

LC = V, J; HC = V, D, J

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16
Q

What activates complement?

A

IgM; IgG

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17
Q

What opsonizes?

A

IgG

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18
Q

What participates in mast cell sensitization?

A

IgE

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19
Q

What is responsible for adding non-germline encoded nucleotides at VDJ junctions?

A

TdT

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20
Q

What kind of immunoglobulins do B cells express?

A

IgG, IgA, and IgE

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21
Q

Which immunoglobulin dimerizes?

A

IgA

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22
Q

What immunoglobulins do naive B cells express?

A

IgM, IgD

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23
Q

Which cells perform cell-mediated cytotoxicity?

A

Natural Killer Cells (NK Cells)

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24
Q

Where is MHC Class I found?

A

Any nucleated cell

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25
Q

What is the length of peptide bound by MHC I?

A

9 AAs

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26
Q

What kind of MHC Class are HLA-DR, HLA-DQ, and HLA-DP?

A

MHC Class II

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27
Q

What kind of MHC Class are HLA-A, HLA-B, and HLA-C?

A

MHC Class I

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28
Q

What is the length of the peptide bound by MHC Class II?

A

Variable

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29
Q

Where are MHC Class II molecules found?

A

APCs and B cells

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30
Q

What is a pre-TCR receptor?

A

TCR beta chain plus the invariable pre-TCRa chain; associates with CD3 signaling complex

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31
Q

What does a pre-TCR do?

A

Blocks further rearrangement of the beta chain; induces proliferation and generates a pool of cells w/ the same beta chain that will subsequently rearrange TCR alpha; induces differentiation into DP

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32
Q

What occurs in TCRa rearrangement?

A

V and J segments rearrange, allowing multiple rounds or recombinations; deletes TCR delta; NOTE: TCRa rearrangement does not immediately block continued recombination

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33
Q

When does TCRa rearrangement stop?

A

TCRa recombination is blocked by recognition of self-MHC complexes during positive selection

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34
Q

Define: Positive T cell Selection

A

The process of rescue from cell death and maturation to SP CD4 or SP CD8 cells upon recognition of MHC-self peptides; occurs in the cortex

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35
Q

Define: Negative T cell Selection

A

TCR receptors that respond too strongly to self-peptide are eliminated (too self-reactive)

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36
Q

How does a T cell decide whether to be CD4 or CD8?

A

If it interacts via TCR w/ an epithelial cell expressing MHC Class I vs. MHC Class II; if it doesn’t react with either, then alpha rearranges and the TCR tries again

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37
Q

What do macrophages secrete?

A

Pro-inflammatory cytokines including IL-6, TNFa, IL-1b, CXCL8, and IL-12

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38
Q

What does IL-6 do?

A

Activate lymphocytes

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39
Q

What does CXCL8 do?

A

Recruits PMN

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40
Q

What are the 2 main cytokine families are their components?

A

Four-helix bundle family of interleukins (IL-2, IL-4, etc AND IFNs) - signal through JAK-STAT; TNF (TNFa, FasL, CD40L AND IL-33) - these signal through the NFkB or Caspase pathway;
NOTE: IL-1, IL-17, and TGFb are NOT part of these families

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41
Q

Define: chemokines

A

Very small secreted proteins that bind ligand-specific G-protein coupled receptors; chemotaxis and chemoattraction is most important; work with integrins to promote cell-specific adhesion

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42
Q

What are the 2 families of chemokines?

A

Homeostatic chemokines (important for creating immune structures; the CCRs; CXCR5); inflammatory chemokines (important for recruiting leukocyte a in response to an immune challenge; pretty much all of the other CXCLs and CXCRs)

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43
Q

What is “the troika” of sepsis?

A

IL-1B, IL-6, and TNFa activation, resulting in activation of complement opsonization, PMN phagocytosis, increased immune response

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44
Q

How does Hepcidin affect the immune system?

A

Hepcidin turns off ferroportin leading to Fe sequestration - elevated Hepcidin can cause Anemia of Chronic Disease! This is b/c both the infection and host want iron for life cycle - battle it out

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45
Q

What does CRP do?

A

Opsonizes bacteria; can be measured clinically as an inflammatory marker

46
Q

What are the 4 types of hypersensitivity?

A

Type I: Immediate - IgE mediated; Type II: Cytotoxic - Ab mediated; Type III: Immune complex mediated; Type IV: delayed-type, T cell mediated

47
Q

Define: Hapten

A

Chemical moiety too small to elicit a T cell response alone, but capable of tight association with self proteins; this “conjugation” creates a new (foreign) target

48
Q

What is sensitization? (As in hypersensitivity)

A

Low-dose allergen exposure often via mucous membranes, resulting in IgE production

49
Q

What is the process of Type I Hypersensitivity?

A

Sensitization; Elicitation (Re-exposure; pre-formed IgE triggers mast cell activation)

50
Q

Define: Mast Cell

A

Subepithelial tissue sentinel of myeloid lineage - major express or of high-affinity receptor for IgE; preformed granules contain histamine

51
Q

What is involved in sensitization response?

A

IgE
Basophils
Mast cells (plasma cell)

52
Q

What is the early phase of sensitization?

A

IgE cross links w/ antigen, releasing preformed mediators (resulting in histamine release, vasodilation, smooth muscle constriction, GI motility, mucous secretion, sensory nerve activation) followed by rapid production of arachnids ice acid products (leukotrienes, prostaglandins)

53
Q

What occurs in the late phase of sensitization?

A

Gene activation and new cytokine production (TNFa recruits inflammatory cells, IL3 and IL5 stimulate eosinophil production, IL4 and IL13 propagate Th2 response)

54
Q

How does immune complex hypersensitivity cause damage?

A

Ag-Ab complexes deposit in local blood vessel walls, fix complement and generate C5a; bind Fc receptors on neutrophils (releasing free radicals and proteases) and platelets (causing aggregation, thrombosis, necrosis)

55
Q

What are the symptoms of serum sickness?

A

Fever; lymphadenopathy; hives; joint pain; proteinuria
These occur about 2 weeks following introduction of long-lived antigen in a naive receptor (like injection of horse serum)

56
Q

What is Delayed-Type Hypersensitivity?

A

Group of T-cell mediated responses to antigen - requires sensitization like Type I, but on re-exposure the reactions occur over 1-3 days; example: poison ivy

57
Q

What do effector T cells produce?

A

Interferon-gamma, chemokines; they recruit macrophages (which produce TNFa)

58
Q

Where is the Hapten taken up if it modifies extracellular proteins?

A

Cutaneous macrophages

59
Q

What is the pathophysiology of atopic dermatitis?

A

Th2 response is increased, decreasing levels of IFN-g, IL2 and increasing IL4 and IL5; IgE, mast cells, and eosinophils are increased

60
Q

What are the major criteria for atopic dermatitis?

A

Must have 3+: pruritis (itching), personal or family history of autopsy, chronic or chronically relapsing dermatitis, typical morphology and distribution

61
Q

What is allergic contact dermatitis?

A

Immune mediated response that requires sensitization, not dose dependent

62
Q

What is irritant contact dermatitis?

A

Not an immune mediated reaction; local, toxic effect on cells that elicits an inflammatory response - can be acute, corrosive, phototoxicity

63
Q

What does IL-1 do?

A

Fever, macrophage activation, activation of vascular endothelium, PMN mobilization

64
Q

What does IL-2 do?

A

T cell proliferation

65
Q

What does IL-3 do?

A

Hematopoietic growth factor for multiplier WBC lineages

66
Q

What does IL-4 do?

A

B cell activation, IgE CSR, Th2 polarization

67
Q

What does IL-5 do?

A

Eosinophil hematopoiesis, chemotaxis, and activation

68
Q

What does IL-6 do?

A

Fever, Th17 differentiation, acute phase reactant induction

69
Q

What does IL-7 do?

A

Proliferation of pre-B and pre-T cells

70
Q

What does IL-10 do?

A

Suppresses APC MHCII and B7 expression

71
Q

What does IL-12 do?

A

Activates NK cells, promotes IFN-g production by macrophages, promotes Th1 polarization

72
Q

What does IL-13 do?

A

B cell proliferation, inhibits macrophage inflammatory cytokine production

73
Q

What does IL-17 do?

A

PMN recruitment and activation

74
Q

What does IL-23 do?

A

Promotes Th17 differentiation

75
Q

What does IFNa do?

A

Proteasome induction, increased MHC I expression

76
Q

What does INFb do?

A

Proteasome induction, increased MHC I expression

77
Q

What does IFNg do?

A

Macrophage activation, increased expression of MHC I and II and antigen processing components, suppression of Th2 polarization

78
Q

What does TNFa do?

A

Neutrophil mobilization, activation of vascular endothelium, increase in vascular leafiness, maturation of DCs, Fever, acute phase reactants

79
Q

What does TGFb do?

A

Inhibits lymphocyte growth and macrophage activation, directs IgA class switch

80
Q

What does GM-CSF do?

A

Hematopoietic growth factor for granulocytes and monocytes

81
Q

What do TNF ligands do?

A

Promote receptor trimerization and NFkB (inflammatory gene expression) and Caspase (programmed cell death) expression

82
Q

What is Autoimmune Lymphoproliferative Syndrome (ALPS)?

A

Rare, often somatic mutation of the FAS gene

Associated profound lymphadenopathy with increased B cells and double negative T cells

83
Q

Why are chemokines desirable drug targets?

A

They signal through G protein coupled receptors (GPCRs)

84
Q

What is the path of a dendritic cell?

A

Antigen taken up by Langerhans cells in the skin, CCR7 increased; L cells go to the lymph system; Mature DC cells transfer antigen to resident DC cells; B7 positive DC stimulate naive T cells; T cells bind to DC through low-affinity LFA-1:ICAM-1 interactions, confirmational change

85
Q

How is a T cell activated?

A
  1. Interacts w/ DC that presents antigen; 2. ZAP-70 kinase; 3. Lots of kinases (NFkB, IP3, NFAT, AP-1); 4. Cell division, proliferation, and differentiation to effector T cells
86
Q

What defines what kind of T cell it will become?

A

A cytokine - Singal #3 (TGFb is Treg; IL6 is TFH; TGFb is TH17, etc)

87
Q

What is needed to activate memory cells?

A

MHC I or MHC II presentation

88
Q

What are the 3 major signals of naive T cell activation?

A
  1. Antigen presentation; 2. APC co-stimulating receptors like CD80/86 activate CD28; 3. Cytokines promote T-cell polarization
89
Q

What are Th1 cells?

A

CD 4 cell that targets intracellular microbes - type I immunity; release IFNg

90
Q

What are Th2 cells?

A

CD4 cells that target helminthes, activate Eos and mast cells; secretes IL-4

91
Q

What is Th17 cell?

A

CD4 cell that targets extracellular microbes, release IL-17

92
Q

What are TFH cells?

A

CD4 cells that are T-cell help for B cells (promoter affinity maturation and class switching)

93
Q

What are Treg cells?

A

CD4 T cells that suppress T-cells directed against self or acquired antigens

94
Q

Why does TB form granulomas?

A

Th1 cells (the “classical” activator of macrophages) surround and partial remove the M. Tuberculosis infected macrophages

95
Q

Why do superantigens cause TSS?

A

Cytokine Storm/exuberant polyclonal T-cell activation; cross-link MHCII to T-cell receptors

96
Q

What do TNF ligands do?

A

Promote receptor trimerization and NFkB (inflammatory gene expression) and Caspase (programmed cell death) expression

97
Q

What is Autoimmune Lymphoproliferative Syndrome (ALPS)?

A

Rare, often somatic mutation of the FAS gene

Associated profound lymphadenopathy with increased B cells and double negative T cells

98
Q

Why are chemokines desirable drug targets?

A

They signal through G protein coupled receptors (GPCRs)

99
Q

What is the path of a dendritic cell?

A

Antigen taken up by Langerhans cells in the skin, CCR7 increased; L cells go to the lymph system; Mature DC cells transfer antigen to resident DC cells; B7 positive DC stimulate naive T cells; T cells bind to DC through low-affinity LFA-1:ICAM-1 interactions, confirmational change

100
Q

How is a T cell activated?

A
  1. Interacts w/ DC that presents antigen; 2. ZAP-70 kinase; 3. Lots of kinases (NFkB, IP3, NFAT, AP-1); 4. Cell division, proliferation, and differentiation to effector T cells
101
Q

What defines what kind of T cell it will become?

A

A cytokine - Singal #3 (TGFb is Treg; IL6 is TFH; TGFb is TH17, etc)

102
Q

What is needed to activate memory cells?

A

MHC I or MHC II presentation

103
Q

What are the 3 major signals of naive T cell activation?

A
  1. Antigen presentation; 2. APC co-stimulating receptors like CD80/86 activate CD28; 3. Cytokines promote T-cell polarization
104
Q

What are Th1 cells?

A

CD 4 cell that targets intracellular microbes - type I immunity; release IFNg

105
Q

What are Th2 cells?

A

CD4 cells that target helminthes, activate Eos and mast cells; secretes IL-4

106
Q

What is Th17 cell?

A

CD4 cell that targets extracellular microbes, release IL-17

107
Q

What are TFH cells?

A

CD4 cells that are T-cell help for B cells (promoter affinity maturation and class switching)

108
Q

What are Treg cells?

A

CD4 T cells that suppress T-cells directed against self or acquired antigens

109
Q

Why does TB form granulomas?

A

Th1 cells (the “classical” activator of macrophages) surround and partial remove the M. Tuberculosis infected macrophages

110
Q

Why do superantigens cause TSS?

A

Cytokine Storm/exuberant polyclonal T-cell activation; cross-link MHCII to T-cell receptors

Immunology (6 decks)

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