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Block 6: Immunology and Inflammation > Week 2 > Flashcards

Week 2 Flashcards

1
Q

TAP

A

peptide transporter that delivers processed, endogenous antigen in to the ER to be complexed with MHC I

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2
Q

polymorphism

A

refers to population level

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3
Q

polygeny

A

refers to individual level

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4
Q

microbial superantigens

A

bind MHC II Class outside of normal binding groove; can cause activation of huge # T cells (10%); nonspecific binding therefore broad activation by binding multiple TCR via b chain, cytokine storm, sepsis

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5
Q

is memory generated against microbial super antigens?

A

no , T cell activation is inappropriate so no mem developed

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6
Q

do microbial superantigens require processing?

A

no

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7
Q

ankylosing spondylitis

A

B27

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8
Q

HLA DQ2 DQ8

A

diabetes type I and also celiac

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9
Q

abacavir

A

drug used in HIV tx that can cause hypersensitivity in indv with HLA B 57 by changing the peptide binding characteristic of MHC II

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10
Q

Carbamazepine

A

anti epileptic that can cause hypersensitivity in HLA B 15

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11
Q

calnexin

A

keeps MHC I alpha stable until B2 binds

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12
Q

calreticulin (a chaperone)

A

keeps MHC I a:b2 stable until TAP bind s

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13
Q

polymorphism

A

population level

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14
Q

polygeny

A

individual level

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15
Q

what c’some are MHC I and MHC II genes on

A

6, with the exception of b2 which is on 15

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16
Q

Peptide anchor residues

A

mediate binding to MHC; side chains of aa residues of peptide that fit into pockets of peptide binding cleft of MHC; peptides that can load a particular MHC are similar in their gene seq, and pretty conserved

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17
Q

IL2R alpha chain

A

CD25

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18
Q

IL2-Receptor

A

present on naive T cells, B cells, NK cells, activated T cells

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19
Q

what pathway does cyclosporin A target

A

TCR-CD3 signaling (by targeting calcineurin calmodulin calcium phosphatase activity)

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20
Q

what can cause SCID besides a RAG1 or RAG2 mutation?

A

deficiency in gamma subunit of the cytokine receptors

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21
Q

class I cytokines

A

2,4,6,12

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22
Q

class II cytokines

A

IFN receptors , IL10

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23
Q

IFN alpha and beta

A

antiviral

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24
Q

IFN gamma

A

macrophage killing, MHC II expression, antiviral responses

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25
Q

thymic aplasia

A

Di George syndrome; no T cells , dcr PTH dir Ca

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26
Q

ex of killed or inactivated vaccine

A

RIP Always (rabies, influenza, polio, hepA)

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27
Q

what attenuates immune response

A

both TGF Beta and IL10

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28
Q

which hypersensitivities are ab mediated

A

I, II, III

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29
Q

things required for class switching

A

happens in germinal centers, requires antigen and MHC and T cell (therefore, requires CD40L - present on T cells, without it can get hyper IgM )

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30
Q

what kind of signaling does class II cytokines use?

A

JAK/STAT

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31
Q

JAK kinases

A

kinases involved in immune response(inhibitors tune down the T cell response)

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32
Q

pre TCR complex

A

following successful rearrangement of B chain for TCR, betaTCR:pTa:CD3 complex signals for stopping beta rearrangement (allelic exclusion), stimulation of proliferation and CD4 CD8 expression, stimulation of alpha chain rearrangement

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33
Q

Homeostatic proliferation

A

t cells in the periphery proliferate (this is why we still have T cells despite our thymus involuting)

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34
Q

B7

A

on APC; binds CD28 on T cells

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35
Q

pleitorpy

A

acts on more than one target

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36
Q

redundancy

A

multiple cytokines act on same cell for the same effect

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37
Q

synergy

A

two cytokines work together to produce a given effect

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38
Q

antagonism

A

one cytokine undoes the action of another cytokine

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39
Q

whats secretes IL1

A

macrophages

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40
Q

phases of DTH

A

sensitization and effector

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41
Q

cd40

A

present on B cells
present on macrophages

therefore without CD40L, T cells can’t communicate with either

42
Q

RORyT

A

expressed by Th17

43
Q

FoxP4

A

expressed by Tregs; without it, get IPEX (immune dysregulation, polyendocrinopathy, enteropathy, X linked)

44
Q

induced t reg function

A

down regulate immune response; generated in periphery

45
Q

innate t reg function

A

maintenance of self tolerance; generated in thymus

46
Q

Bcl6

A

expressed by TFH

47
Q

Follicular helper T cells

A

TFH; express Bcl6; secrete Il21, express ICOS ; help B cells during germinal center reaction (class switching and somatic hypermutation)

48
Q

CXCR5

A

expressed by resting B cells

49
Q

CCR7

A

expressed by resting T cells

50
Q

major killing pathway for CD8+ cells

A

perforin/ granzyme mechanism

51
Q

minor killing pathway for CD8+ cells

A

FAs ligand to induce apoptosis

52
Q

what is the common end point of perforin/granzyme and Fas pathways

A

activate procaspase into caspase which can activate apoptotic factors

53
Q

type 1 hypersensitivity

A

IgE, mast cell activation, soluble antigen, systemic anaphylaxis, acute urticaria, seasonal rhinoconjuncitvitis, asthma and food allergy, asthma

54
Q

type 2 hypersensitivity

A

IgG, cell or matrix associated antigen; FcR cells = phagocytes, NK cells; complement

55
Q

what kind of rxn is against penicillin

A

type 2 hypersensitivity

56
Q

what kind of rxn is against TB

A

type 4 hypersensitivity

57
Q

what type of hypersensitivity is for serum sickness

A

3

58
Q

what type of hypersensitivity is for arthus

A

3

59
Q

what do type I II and III hypersensitivities have in common

A

all are antibody mediated

60
Q

what kind of reaction is poison ivy

A

type 4 CTL mediated hypersensitivity

61
Q

what kind of cell will bind IgE

A

mast cell!!!

62
Q

why is it that upon first exposure of antigen nothing may happen?

A

because during sensitization you create the antibodies (IgE) that can bind to the mast cells. But just the IgE binding to the mast cell does not trigger degranulation; it is the mast cells expressing IgE that then come in contact with the specific antigen that will cause degranulation; this is also why if you are developing an anti-IgE antibody to mediate allergic rxns you need to be only targeting soluble IgE because if you cross link the IgE thats already bound to the mast cell then you will actually promote degranulation and anaphylaxis

63
Q

can mast cells secrete interleukin?

A

yes they secrete Il4 which amplifies IgE production

64
Q

name as many things as you can that mast cells can release

A 
histamine
heparin 
tryptase
carboxypeptidase
cathepsin 
Il4 
Il13
Il3
Il5 
GMCSF 
TNF alpha 
CCL3 
prostaglandins
leukotriene
platelet activating factor
65
Q

what can present haptens

A

haptens need carriers; can be taken up by langerhans

66
Q

tissue transglutaminase

A

modifies gluten so that it can bind MHC II –> celiac (activated CD4+ cells can bind FAS and kill epithelial cell

67
Q

FUT 1 mutation

A

no H antigen; bombay phenotyp

68
Q

FUT 2 mutation

A

80% ofpeople have polymorphism that causes presence of ABO in secretions

69
Q

Intravascular hemolytic transfusion reaction

A

IgM complement fixation

70
Q

Extravascular hemolytic transfusion reaction

A

IgG phagocytosis

71
Q

isohemagglutinins

A

naturally occurring IgM antibodies to A or B antigens

72
Q

ABO typing

A

erythrocytes are typed for their ABO antigens

73
Q

reverse typing

A

serum is typed for its ability to agglutinate erythrocyte of various blood groups

74
Q

test results in hemolytic disease of new born

A

positive direct and positive indirect coombs test

75
Q

indirect coombs test

A

detects circulating antibodies and is typically performed on the serum from the mother.

76
Q

direct coombs test

A

detects antibodies which are already found on the surface of the erythrocytes and is typically performed on the red blood cells of the foetus or the newborn.

77
Q

glucuronidation

A

how to make bilirubin more excretable; in newborn’s this is generally less efficient and so bilirubin tends to accumulate more than in adults (newborn jaundice is not uncommon)

78
Q

BBB of newborn

A

more permeable

79
Q

kernicterus

A

brain damage due to excess bilirubin in the brain

80
Q

bilirubin

A

degradation product of hemolysis

81
Q

hemolytic disease of the newborn

A

IgG antibodies form mom cross placenta and react with Rh+ fetal erythrocytes causing extravascular hemolysis!!! especially in spleen; anemia, jaundice, kernicterus

82
Q

bili light

A

phototherapy that involves exposure of baby to blue greenn light spectrum to convert bilirubin to water soluble isomer to promote excretion

83
Q

how does IFN gamma activate macrophages

A

inducing iNOS

84
Q

w/o macrophages what kind infection susceptible to?

A

myobacterium

85
Q

what phosphorylates ZAP 70

A

Lck

86
Q

what process is ZAP 70 involved

A

TCR:CD3 signaling pathway –> NFAT activation and IL2 production for T Cell stimulation and proliferation

87
Q

what interleukin can promote antibody production

A

Il4

88
Q

what immunoglobulin is important in parasite infection

A

IgE

89
Q

TDAP vaccine

A

tentanus, diphtheria and pertussis

90
Q

what can measles bind

A

binds to a regulator of the complement system

91
Q

Tetanus Immune Globulin (TIG)

A

recommended for tetanus treatment and prophylaxis against tetanus following injury in patients whose tetanus immunization is incomplete or uncertain.

92
Q

why do you not give TIG to immunized patients?

A

spores need to germinate, which takes time, so by the time the secondary response kicks in (2-3 days ) its still soon enough to be before the spores germinate

93
Q

how many doses is MMR vaccine

A

2

94
Q

oral polio virus

A

live, attenuated

95
Q

polio shot

A

killed virus

96
Q

measles shot

A

live, attenuated

97
Q

Thimerosol

A

mercury based preservative, helps prevent growth and spread of bacteria; human body can easily clear thimerosol. Furthermore, the amount is so small, that, in conjunction with the rapid clearance from the body, never builds up!

98
Q

what vaccines are contraindicated in peds onc patient

A

live, attenuated; MMR and Varicella (chicken pox)

99
Q

Varicella

A

chicken pox

100
Q

how long does passive immunity last

A

3-6 mo

101
Q

how do you decide whether to give an HIV patient a vaccine?

A

depends on CD4 count! <200 do not give

102
Q

what is chronic rejection characterized by

A

reactions in vasculature of the graft; often see inflammation that thickens vessel, therefore narrowing lumen and causing loss of function

Block 6: Immunology and Inflammation (6 decks)

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