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FMS > FMS Week 8 > Flashcards

FMS Week 8 Flashcards

Immunology

1
Q

What are T regulatory cells?

A

suppress Th1 and Th2 and have an anti-inflammatory effect

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2
Q

What is the general result of deficiency in classical pathway components?

A

autoimmune disease

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3
Q

What is IL-4?

A

the major Th2 cytokine; activates Th2/suppresses Th1 production; promotes IgE production (parasites)

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4
Q

What additional binding is required for B-cell class switching in T-cell dependent activation?

A

CD40 (B-cells) to CD40 Ligand (T-Cells)

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5
Q

What does CRP bind to?

A

CRP joins the C1 complex to Bacterial polysaccharides

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6
Q

Describe the classical complement pathway

A

The C1 complex binds to CRP; the attaching of 2 adjacent Fc complexes removes C1-inh, activating C1r & C1s (proteases); C4 and C2 are cleaved; C4b and C2b create a C3 convertase; C3 convertase generates C3b

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7
Q

What proteins make up the membrane-attack complex?

A

C5b, C6, C7, C8, C9

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8
Q

what are interleukins?

A

cytokines that travel between leukocytes

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9
Q

Which antibodies are dimers?

A

IgA

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10
Q

what are cytokines?

A

cell signalling proteins that stimulate inflammatory response

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11
Q

What are the 3 key functions of macrophages?

A

phagocytosis, cytokine production, antigen presentation

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12
Q

What are the functions of antibodies?

A

opsonization, neutralization, activating complement

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13
Q

What are kupffer cells?

A

macrophages of the liver

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14
Q

What is DAF?

A

decay accelerating factor (CD55); disrupts C3b attachment in formation of C5 convertase; protects host cells from late complement pathway

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15
Q

What is the secretory component?

A

the bridge that links IgA monomers as they pass through epithelial cells creating a dimer in secretions

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16
Q

What are the key roles of Natural Killer Cells?

A

Kill virus-infected cells; produce INF-γ to activate macrophages

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17
Q

what cells are agranulocytes?

A

Lymphocytes (NKC, T & B) and monocytes (macrophages)

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18
Q

What are the properties of C5a?

A

Anaphylatoxin and neutrophil chemotaxis

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19
Q

What types of molecules do T-cells recognize?

A

only peptides presented by APCs

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20
Q

what is the difference between mast cells and basophils?

A

basophils are found in the blood stream, and mast cells are in the tissue

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21
Q

What is IL-1?

A

a cytokine released by macrophages; increases synthesis of endothelial adhesion molecules allowing neutrophils to enter inflamed tissue; acts as an endogenous pyrogen by acting on the hypothalamus

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22
Q

What are PAMPs?

A

pathogen-associated molecular patterns; present on many microbes but not human cells, used by the immune system to recognize pathogens

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23
Q

Describe the alternative complement pathway

A

Spontaneous conversion of C3 to C3b; stabilized by amino and hydroxyl groups on bacterial surfaces; stabilized C3b binds to Factor B (C3bB); Factor D clips Factor B to make C3bBb (C3 convertase); C3 convertase can make more C3b leading to rapid accumulation on surfaces

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24
Q

How do nucleic acids act as PAMPs?

A

DS-RNA and Unmethylated DNA are characteristic of pathogens and recognized by the innate immune system

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25
Q

What is the LPS pathway:

A

LPS binds LPS-binding protein of plasma; complex binds CD14 on macrophages, triggers TLR4 which produces cytokines (IL-1, IL-6, IL-8, TNF)

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26
Q

what are chemokines?

A

cytokines that attract immune cells (chemotaxis)

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27
Q

What is the structure of MHC class I?

A

One heavy chain (alpha) and one microglobulin (beta)

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28
Q

Which antibodies are pentamers?

A

IgM

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29
Q

What are the components of the c1 complex?

A

C1q, C1r, C1s, and C1-inh

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30
Q

What is Factor H?

A

Plasma glycoprotein that protects host cells from alternative compliment pathway: accelerates decay of C3 convertase, inactivates C3b; some pathogens/cancers have developed the ability to use endogenous Factor H for evasion

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31
Q

What are the unique characteristics of the adaptive immune system?

A

Slow acting (days), highly specific, memory, requires antigen presentation

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32
Q

What are Th1 cells?

A

CD4 T-cells that drive “cell-mediated” immunity and promote specific IgG subclasses

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33
Q

How does mannose act as a PAMP?

A

Binds MBL (mannose-binding lectin) from the liver and activates the lectin pathway of complement

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34
Q

What is IL-10?

A

a Th2 cytokine; inhibits Th1 production; anti-inflammatory

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35
Q

Describe T-cell maturation

A

immature T-cells migrate from bone marrow to thymus; express TCR, bind to self MHCs; only “ideal” TCR cells survive (positive selection in cortex, negative in medulla)

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36
Q

Why is IgM the best activator of compliment?

A

the C1 proteins of the Fc regions are positioned closer together

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37
Q

How does ADCC work in Eosinophils?

A

IgE binds to pathogens, Eosinophils bind IgE (Fc), release toxic enzymes onto parasite

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38
Q

What is the significance of protein A?

A

part of some bacterial cell walls (Staph Aureus); binds Fc portion of IgG (preventing opsonization and compliment activation)

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39
Q

What is IFN-γ?

A

a cytokine from Th1 that increases MHC expression: activates Th1/suppresses Th2 production; activates macrophages

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40
Q

What is the role of neutrophils?

A

“back up” called in by macrophages; extra phagocytosis

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41
Q

what is the role of CD8 T-cells?

A

cytotoxic (Tc); kills virus-infected and tumor cells

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42
Q

How does tuberculosis block phagocytosis?

A

modifies phagosome so it cannot fuse with lysosome, leading to proliferation inside macrophages and protection from antibodies

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43
Q

What are TLRs?

A

toll-like receptors; a class of pattern recognition receptors on Macrophages, dendritic cells, and mast cells that recognize PAMPs and then secrete cytokines

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44
Q

What is CD59?

A

MAC inhibitory protein; disrupts formation of the MAC; protects host cells from late complement pathway

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45
Q

describe the co-stimulation of CD8 Tc?

A

TCR binds to antigen (on MHCI) and CD8 binds to MHCI; also IL-2 from Th cells

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46
Q

How are eosinophils stimulated?

A

IL-5 from Th2 cells

47
Q

What is IL-2?

A

cytokines mostly from Th1 cells that are T-cell growth factors and lymphocyte activators

48
Q

What is Chediak-Higashi Syndrome?

A

immune deficiency where lysosomes cannot fuse with phagosomes leading to recurrent bacterial infections

49
Q

What is the purpose of multiple C genes in antibodies?

A

different C genes encode alternative antibody classes

50
Q

What is LPS?

A

endotoxin; a PAMP; binds LPS-binding protein of plasma

51
Q

What are the anaphylatoxins (inflammatory proteins) of the complement system and their relative potency?

A

C5a>C3a>C4a

52
Q

Why is IgM always the default?

A

First C gene in the sequence; change requires alternative splicing

53
Q

Describe neutrophil “rolling”:

A

selectin ligands on neutrophils bond to E-selectin or P-selectin of endothelial cells (stimulated by IL-1 and TNF during inflammation) and slow down

54
Q

By what means does C3b lead to attack of bacteria?

A

Directly by opsonization; indirectly by activation of late pathway via C5 convertase

55
Q

What is IgA protease?

A

bacterial enzymes that cleave the secretory component and allow colonization of mucosal surfaces

56
Q

Why is IgM a weak opsonin?

A

Receptors cannot access Fc regions

57
Q

What is somatic hypermutation?

A

Following mutations in V,D,J genes: B-cell receptors with stronger antigen binding proliferate more

58
Q

What is required for T-cell dependent activation of B-cells?

A

receptor crosslinking; T cell binding

59
Q

What is the most common manifestation of deficiency in DAF or CD59?

A

hemolysis of RBCs

60
Q

What antibodies can cross the placental barrier?

A

only IgG

61
Q

Describe neutrophil “crawling”:

A

the integrins of neutrophils (stimulated by LPS and C5a) bind ICAM on endothelial cells

62
Q

What is ADCC?

A

antibody-dependent cellular cytotoxicity

63
Q

What is the CD3 complex?

A

complex surrounding the alpha and beta chains of T-cell receptor that transmits “bound” signal into the cell

64
Q

Why is CRP considered an “acute phase reactant”?

A

It activates the early classical pathway(C1-C4), but does not activate the late pathway (C5-C9)

65
Q

What is the major antibody of secondary response?

A

IgG

66
Q

What are Th2 cells?

A

CD4 T-cells that drive “humoral” immunity and activate B-cells to produce IgE/IgA antibodies

67
Q

What happens to human cells with reduced MHC I?

A

killed by NKCs

68
Q

What is inside the lysosomes of macrophages?

A

reactive oxygen species and nitrogen intermediates produced by NADPH Oxidase (respiratory burst); digestive enzymes

69
Q

What genes make up the B-cell receptor?

A

Variable portion:V,D,J

Constant portion: C

70
Q

What are the 2 types of activated B-cells?

A

plasma (antibody making) and memory (only in T-cell dependent)

71
Q

What are Th17 cells?

A

Subset of CD4 that produces IL-17 to recruit neutrophils and macrophages; protect against GI bacteria and autoimmunity

72
Q

What is the role of CD4 T-cells?

A

helper (Th); produces cytokines to stimulate B-cells, CD8 Tc, and macrophages

73
Q

What are microglia?

A

macrophages of the CNS

74
Q

What antibody is the most abundant in plasma?

A

IgG

75
Q

What composes MHC class II?

A

alpha and beta chains; invariant chain in ER; peptide antigens on the surface

76
Q

How do neutrophils “transmigrate”?

A

tightly bound (crawling) neutrophils bind PECAM-1 between endothelial cells

77
Q

What are phagocytes?

A

immune system cells that directly eat pathogens which enter the body; macrophages and neutrophils

78
Q

What is the most abundant complement protein?

A

C3

79
Q

What do NOD receptors do?

A

NOD receptors bind peptidoglycans of bacterial cell walls when they enter a cell, then secrete cytokines

80
Q

What factors contribute to genetic variation of B-cell receptors?

A

V,D,J genes on chromosome 14 of heavy chain; V/J gene rearrangements on the light chain

81
Q

What cleaves C5 into C5a and C5b?

A

C3b

82
Q

How are CD4 Th activated?

A

MHC Class II of APCs binds CD4

83
Q

What opsonins are associated with neutrophils?

A

only IgG

84
Q

What are the steps of neutrophil blood stream exit?

A

rolling, crawling, transmigration, migration to site of inflammation (chemokines)

85
Q

What disease is associated with C1-inh defects?

A

hereditary angioedema

86
Q

What is TNF?

A

tumor necrosis factor; cytokine that causes tumor death

87
Q

Which antibodies are monomers?

A

IgD, IgE, IgG

88
Q

What is IL-5?

A

a Th2 cytokine; activates eosinophils; promotes IgA production (GI bacteria)

89
Q

What are band forms?

A

immature neutrophils seen in bacterial infections due to extra active bone marrow production; referred to as “left shift”

90
Q

What are Natural Killer Cells?

A

the lymphocytes of the innate immune system

91
Q

How does ADCC work in NKCs?

A

CD16s are crosslinked by binding to IgGs (Fc) of antibody covered infected cells, leading to degranulation into a lytic synapse

92
Q

Describe T-cell independent activation of B-cells

A

Requires very strong antigen crosslinking; important for non protein antigens; weaker response (mostly IgM, no memory)

93
Q

Where do complement proteins bind the B cell receptor?

A

CH2 region of heavy chain

94
Q

What disease is associated with DAF or CD59 defects?

A

paroxysmal nocturnal hemoglobinuria

95
Q

What is the difference between macrophages and monocytes?

A

monocytes circulate in the blood, are referred to as macrophages if they enter the tissue

96
Q

What surface proteins are important for B-cells?

A

CD40, MHC Class II, B7 (binding with T-cells)

CD19 (all), CD20 (most, not plasma), CD21 (compliment, EBV)

97
Q

What is IL-12?

A

cytokine from macrophages that stimulates Th1 production

98
Q

What chemotaxins are associated with neutrophils?

A

IL-8 from macrophages and C5a from complement

99
Q

What is the key difference between MHC classes I and II?

A

MHC I is found on all cells (presents to CD8s); MCH II is only on APCs (presents to CD4s)

100
Q

How are macrophages activated?

A

PAMPs via surface TLRs, IFN-γ from T-cells & NKCs, C5a from complement

101
Q

What are interferons?

A

cytokines that interfere with viral replication

102
Q

What is TNF-α?

A

a cytokine released by macrophages; can cause vascular leak (septic shock); inhibits lipoprotein lipase (cachexia); kills tumors via intravascular coagulation of tumor cells

103
Q

What cells are antigen presenting cells?

A

dendritic cells, macrophages, and B-cells

104
Q

How do CD8 Tc kill virus infected cells?

A

insert perforins (form channels in cell membrane); insert granzymes (degrade cell contents and activate caspases); insert granulysin (lyses bacteria); produces Fas ligand (extrinsic apoptosis)

105
Q

Describe the Lectin Pathway

A

Circulating MBL and MASPs bind to the mannose-containing surfaces of microbes; complement proteins C2 and C4 come in and are cleaved into C2b and C4b which bond to create a C3 convertase (C4b2b); C3 convertase creates C3b

106
Q

Neutrophil small granules vs larger granules

A

Small granules are secondary and are found in both lysosomes and extracellular space; larger granules are only in lysosomes

107
Q

What disease is associated with defects in factor H?

A

age-related mascular degeneration and atypical hemolytic uremic syndrome

108
Q

What cells are granulocytes?

A

neutrophils, eosinophils, basophils, and mast cells

109
Q

Characteristics of IgE

A

defense against parasites (eosinophils and mast cells); low plasma concentration; no complement

110
Q

What are dendritic cells?

A

antigen presenter cells of the skin and mucosal membranes; migrate to the lymph nodes to activate T-cells

111
Q

Describe CD4 T-cell co-stimulation:

A

TCR binds antigen (on MHCII); CD4 binds MHCII; CD28 binds B7 protein of APC

112
Q

what cells are activated by Th1s?

A

CD8 Tc and macrophages

113
Q

Characteristics of IgA

A

Does not fix complement (no inflammation); secreted in mucous; coats pathogens so they cannot invade

114
Q

What stimulates production of CRP?

A

IL-6 from macrophages

FMS (10 decks)

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