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Block 6: Immunology and Inflammation > Week 3 > Flashcards

Week 3 Flashcards

1
Q

arthus reaction

A

type III IgG mediated hypersensitivity; occurs at skin ; can occur if too many boosters are given; reaction against antigen antibody complex

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2
Q

reaction against penecillin

A

type II IgG mediated hypersensitivity

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3
Q

serum sickness

A

type III IgG mediated hypersensitivity; IgG neutralizes ag, forming Ag-ab complexes; get IgG and C3 deposits due to excessive cross linking

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4
Q

hapten

A

an antigen with a single epitope; needs a carrier to be immunogenic

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5
Q

urticaria and serum sickness

A

urticaria is associated with complement activation because C3a and C5a are anaphylacticin (stimulates anaphylaxis)

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6
Q

vasculitis and serum sickness

A

vasculitis occurs because the antigen antibody complexes deposit in small blood vessels, which causes hemorrhaging or damage to these vessels resulting in purpuric lesions

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7
Q

genetic component to celiac

A

HLA DQ8 and DQ 2 genes

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8
Q

celiac immune mech

A

type IV hypersensitivity reaction but its actually technically not an autoimmune disease because the antigen is exogenous

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9
Q

what is the enzyme with abnormal activity in celiac disease?

A

tissue transflutaminase

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10
Q

what is the mechanism of presentation of gluten “antigen”

A

MHC II / CD4+

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11
Q

Fc eRI

A

high affinity Fc receptor present on mast cells; the Fc of IgE will bind here and cause mast cell to release Il4 which increases the secretion of IgE by the plasma cell

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12
Q

where are the key areas that are affected by mast cell degranulation

A

GI
eyes, nose, airways
blood vessels

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13
Q

impact of mast cell on GI

A

causes increased fluid secretion, incr peristalsis; expulsion!!! (diarrhea or vomiting)

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14
Q

impact of mast cells on eyes nose and airways

A

decreased diameter and increased mucus secretion; congestion, swelling and mucus secretion in nose

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15
Q

impact of mast cells on vessels

A

incr blood flow, incr permeability

can lead to hypotension and anaphylactic shock

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16
Q

what enzymes do mast cells have and what do they do

A

remodel connective tissue matrix; cathepsin, chemise, tryptase

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17
Q

omalizumab

A

anti-IgE antibody

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18
Q

Th1

A

IFN gamma , make macrophages angry

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19
Q

hyper acute response

A

within minutes due to pre-existing recipient antibodies reacting to donor antigen; type II hypersensitivity and activate complement

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20
Q

what causes GVHD

A

alloreactive effector T cells from the donor that attacks normal tissue;

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21
Q

what kind of hypersensitivity rxn is hyper acute rejection?

A

type II

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22
Q

what kind of hypersensitivity rxn is acute rejection

A

type IV

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23
Q

what kind of hypersensitivity reaction is chronic rejection

A

type II and type IV

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24
Q

clinical manifestation of GVHD

A

rash and diarrhea

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25
Q

effector fxns of macrophages (5)

A 
phagocytosis
opsinizaiton (binding constant aspect of antibodies)
antimicrobial 
secretion of factors (TNFalpha, Il6) 
Antigen processing and presentation
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26
Q

shape of dendritic cell in tissue

A

expanded

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27
Q

shape of dendritic cell in circulation

A

round

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28
Q

shape of dendritic cell when presenting antigen

A

extend thin processes

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29
Q

how do dendritic cells enter lymph node?

A

through afferent lymphatic vessels to the outer cortex

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30
Q

CD141+ cells

A

conventional dendritic cells found in blood and secondary lymphoid organs

produce lots of IL12

do cross presentation

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31
Q

CD123+ cells

A

plasmacytoid dendritic cells (the major producer of type I interferons, alpha beta)

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32
Q

class I cytokine receptors

A

IL246 12 , JAK, STAT

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33
Q

class II cytokine receptors

A

IFN alpha beta and gamma

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34
Q

what should you associate IFN gamma with

A

TH1, activation of macrophages

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35
Q

CCR5

A

tells dendritic cell to go to periphery and be resident there

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36
Q

CCR7

A

after DC has encountered antigen, this chemokine tells it to go to the draining lymph node

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37
Q

as the DC goes to the lymph node with antigen, what does it do to mature?

A

up regulated MHC I and MHC II, up regulate costimulatory molecules, up regulate adhesion molecules , acquire the ability to produce pro-inflammatory cytokines

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38
Q

what do cDCs express in the resting states

A

MHC II in INTRACELLULAR stores

little to no costimulatory molecules

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39
Q

upon maturation, what do cDCs express?

A

MHC II in PLASMA MEM
ICAM
LFA1
CD80/CD86 (B7.1 and .2)

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40
Q

how do dendritic cells present to CD8 cells if not infected themselves?

A

cross presentation

or transfer of antigen from an infected dendritic cell to a non infected dendritic cell

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41
Q

which DC is main producer of IFN alpha

A

plasmacytoid DC

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42
Q

which DC is main producer of IFN beta

A

conventiona myeloid l DC

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43
Q

what kind of cell expresses CD28

A

CD28 is constitutively expressed on T cells

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44
Q

what does triggering of CD28 induce?

A

T cell proliferation
IL2 production
T cell survival

(NFKB!)

very important but not ~absoluteyl necessary for survival~ b/c in absence, have weakened but not totally wiped out t cell activation

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45
Q

what other molecule in addition to CD28 is imp for NFKB pathway

A

PKC theta

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46
Q

ICOS

A

especially important for germinal center T cells –> T follicular helper cells that help B cells

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47
Q

what kind of cells express PD-1

A

activated T and B cells, macrophages

when bound to ligand, decrease downstream signaling of T cells and reduce T cell proliferation, survival and Il2 production

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48
Q

immune checkpoint blockade

A

prevents the induction of tolerance of T cells, or inhibition of activation by DCs of T cells

this means DCs can activate T cells

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49
Q

immune checkpoint

A

CTLA-4 and PD-1

both are inhibitory to T cell proliferation, survival and Il2 production

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50
Q

what kinds of cells can produce IL4

A

Ancillary mast cells
basophils
T cells

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51
Q

what induces Tregs to become Tregs

A

TGF beta

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52
Q

why are TFH so great at helping B cells make antibodies

A

because they have the right costimulatory molecule (ICOS)

and the right chemotactic to get to the germinal center (CXCR5)

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53
Q

AIRE

A

allows expression of peripheral tissue antigens to be presented in the thymus; induces tolerance to the endocrine organs (pancreas, thyroid…)

without it, get APS = autoimmune polyglandular syndrome

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54
Q

addisons disease

A

adrenal insufficiency, clinical manifestation of AIRE impairment aka APS

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55
Q

clinical manifestations of ALPS

A

hypothyroidism, hypoparathyroidism, diabetes, addisons disease (adrenal insufficiency)

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56
Q

tolerogenic conditions

A

induce tolerance
therefore –> induce apoptosis or anergy
therefore–> signal 1 without signal 2 (apoptosis)
OR signal 1,2 without 3 (anergy)

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57
Q

what kinds of cells induce tolerance

A

resting DCs (low costimulatory molecules)

absence of adjuvant (APCs not activated)

presentation of cells that are not APCs (no costimulatory molecules)

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58
Q

signal 1

A

MHC:peptide

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59
Q

signal 2

A

costimulatory molecule (like CD80/86:CD28)

60
Q

signal 3

A

pro inflammatory cytokines

61
Q

In the absence of T cell help B cells are ____

A

anergized

62
Q

what signals do B cells require to activate?

A

antigen:BCR

T cell co-stimulation (CD40L:CD40 )

63
Q

what can absence of Tregs lead to?

A

IBD and hemolytic anemia

64
Q

EAE

A

experimental autoimmune encephalitis; experimental model of MS

65
Q

what is oral tolerance mediated by?

A

TGF beta producing T regs

66
Q

how is the tolerogenic process sustained?

A

Tregs induce tolerogenic DCs

67
Q

does RA involve antibodies or T cells

A

auto reactive T cells

68
Q

does diabetes involve antibodies or T cells

A

auto reactive T cells

69
Q

does MS involve antibodies or T cells

A

auto reactive T cells

70
Q

does SLE involve antibodies or T cells

A

both

71
Q

does hashimotos involve antibodies or T cells

A

both

72
Q

does graves involve antibodies or T cells

A

antibodies

73
Q

does Sjogrens involve antibodies or T cells

A

both –> against ribonucleoprotein

74
Q

genetic susceptibility to autoimmunity

A

GENES FOR

1) HLA
2) clearance of apoptotic cells (self presented without anti-inflame signals)
3) TCR/BCR signaling
4) neg regulation (ex: CTLA4)
5) Lymphocyte apoptosis (no Fas, no killing of bad stuff)

75
Q

what do infections have to do with autoimmunity?

A

they can be the trigger or ADJUVANT

76
Q

molecular mimicry

A

exposure to antigen that is super close to self-ag that initially the immune response is against the antigen but then it becomes against self (ex: Rheumatic fever )

77
Q

APS

A

AIRE defect

78
Q

ALPS

A

Fas defect; lympho-proliferative disorder in which failure of inducing apoptosis in T and B cells leads to accumulation of auto-reactive and abnormally activated lymphocytes.

79
Q

key examples of monogenic autoimmunity

A

Defect in:

AIRE (APS)
Fas (ALPS) 
FOXp3 (Tregs --> IPEX) 
CTLA4 (graves, type 1 diabetes) 
C1q (SLE)
80
Q

two key mechanisms of autoimmunity

A

auto-antibodies

auto reactive T cells

81
Q

anti-chromatin antibodies

A

diagnostic for lupus

82
Q

anti-nucleolar

A

diagnostic for scleroderma

83
Q

what are some methods to detect autoantibodies?

A

ELISA or immunofluorescence

84
Q

Ab-Dependent Cell-mediated Cytotoxicity (ADCC)

A

NK cells, neutrophils, eosinophils, macrophages and monocytes can kill opsonized cells using several mechanisms:

1) release of cytolytic granules containing perforin and granzymes like the CTLs
2) or other lytic enzymes like the neutrophils
3) or through the production of pro-apoptotic cytokines like the TNFa secreted by macrophages.

85
Q

ADCC is a classic example of

A

adaptive immune system assisting the innate cells in clearing pathogens.

86
Q

Goodpastures

A

AutoAbs deposit along the glomerular basement membrane; the autoantibodies are against the basement membrane collagen Type IV of the glomeruli in the kidney => glomerulonephritis

87
Q

what pathology is due to stimulating autoantibodies

A

graves

88
Q

what autoimmune pathology is due to direct cell damage

A

goodpastures

89
Q

clinical manifestation of graves

A

hyperthyroidism

90
Q

what autoimmune pathology is due to blocking autoantibodies

A

myasthenia gravis

91
Q

myasthenia gravis

A

auto-antibodies bind Ach receptors on the skeletal muscle –> blocks binding of natural ligand acetylcholine and the transmission of the nervous signals;

also induces internalization and degradation of the receptors

92
Q

clinical manifestation of myasthenia gravis

A

inhibition of skeletal muscle contraction and weakness.

93
Q

4 ways that autoantibodies are pathogenic

A

1) direct cell damage (good pastures)
2) stimulating autoantibodies (graves –> hyperthyroidism0
3) blocking autoantibodies (myasthenia gravis –> muscle weakness)
4) immune complex (SLE which is type III hypersensitivity)

94
Q

what kind of hypersensitivity is lupus

A

type 3

95
Q

T cell help is required for

A

IgG autoantibody production

96
Q

insulitis

A

destruction of islets of langerhans by CTLs, infiltration by CD4, DC and macrophages

97
Q

what kind of T cell in hashimotos?

A

Th1

98
Q

what gender is hashimotos more common in?

A

women

99
Q

are their autoantibodies in hashimotos?

A

yes, it is an autoimmune disease involving both B and T cells; the auto-antibodies are against thyroid things like thyroid peroxidase and thyroglobulin

100
Q

muscle weakness, ataxia, blindness and limb paralysis

A

MS

101
Q

what are the antigens in MS

A

myelin basic protein, MOG (myelin oligodendrocyte glycoprotein)

auto-reactive T cells kill these and destroy myelin sheath

102
Q

what stimulates innate immune cells in the beginning of RA

A

TLR

103
Q

fibroblast-like synoviocyte

A

activated by TNF alpha and IL6; produce matrix metalloproteases and express RANK-L thereby activating osteoclasts

104
Q

rheumatoid factor

A

IgM antibody to the Fc part of IgG

105
Q

peptidyl arginine deaminase

A

PAD; inducible enzyme in RA that causes argnini to be changed to citrulline (removes charge); autoantibodies to citrulinnated peptides are found in 90% RA patients

106
Q

ACPA

A

anti-citrillunated peptides autoantibodies

107
Q

imp examples of citrulinated self peptides

A

citrullinated epitopes on fibrinogen, vimentin, fibronectin, collagen, enolase, and histones.

can induce NETosis!

108
Q

4 tx options for autoimmunity

A

1) replacement therapy
2) general immunosuppression
3) targeted immunosuppression
4) re-establish normal tolerance (still experimental)

109
Q

histocompatibility

A

the property of a tissue to be accepted and not rejected by the immune system

110
Q

chronic rejection

A

vasculitis

111
Q

hyperacute

A

antibody mediated

112
Q

mandatory step to prevent hyperacute rejection

A

testing ABO in donor and recipient

113
Q

what kind of hypersensitivity is the hyperacutre rejection

A

type 2

114
Q

cross matching

A

screen recipients serum for antibodies against HLA

115
Q

what assays are used for cross matching

A

complement dependent cytotoxicity (CDC)
flow cytometric crossmatch
Luminex (solid-phase assay)

116
Q

PRA = panel reactive antibody

A

allows estimation of the percentage of the population against which a candidate has pre-formed anti-HLA antibodies

part of cross matching a transplant candidate

117
Q

how do you desensitize recepient to a xenograft?

A

plasmapheresis and administration of intravenous immunoglobulins

118
Q

molecular test to detect the DNA sequence of the HLA alleles

A

PCR

119
Q

Mixed Leukocyte Reaction (MLR)

A

determines the strength of the response of the host/recipient T cells against donor cells in vitro. (takes 5 days)

120
Q

what does anti-CD3 block?

A

signal 1

121
Q

cross presentation

A

phenomenon of dendritic cells presenting on MHC Class I to CD8+ T cells Ags acquired from other cells (usually cells that went into apoptosis)

122
Q

what activates apc in transplant?

A

danger signals introduced by surgeon and trauma

123
Q

survival of mature dendritic cells and why its important

A

3-4 days; this is why direct recognition in transplant happens early and indirect recognition is more important later

124
Q

AMR

A

antibody mediated rejection; can be preformed or CD4+ T cells that participate in indirect recognition can activate B cells to produce antibodies against the graft

125
Q

T cells in presence of ___ and ___ can help B cells make antibodies

A

Il2 and Il4

126
Q

TSA

A

tumor specific antigen; a “new” or “mutated self” expressed on tumor cells (Bcr:Abl)

127
Q

TAA

A

tumor associated antigen; a protein that is expressed on normal cells in low amounts or on fetal cells that becomes upreg or expressed on tumor cells

128
Q

Burkitt’s lymphomas

A

translocated c-myc gene (c-myc is example of TAA that can get unregulated in cancer cells)

129
Q

NK cell surface profile

A

CD3- CD4- CD8- CD16+

130
Q

CTL surface profile

A

CD3+ CD4- CD8+ CD16-

131
Q

how do NK cells recognize tumor?

A

they do not recognize TSA or TAA, instead they note the lack of MHC; they are not specific in their response; they are part of innate immunity, first line of defense, no memory

132
Q

How do CTL cells recognize tumor?

A

acquired immunity, delayed but SPECIFIC response; they get sensitized, create memory and have a clonotypic antigen receptor; respond to TSA or TAA

133
Q

what can have decreased MHC?

A

virus infected cell or tumor cell; this is very important because this causes NK cell to kill it but also prevents the foreign antigen from being presented to T cell

134
Q

in what diseases are all Ig classes low

A

bare lymphocyte, bruton’s x linked agammaglobulinemia , common variable hypogammaglobulinemia

135
Q

Wiskott Aldritch

A

IgM low, IgG normal, IgE and IgA ElevAted

136
Q

Ataxia talengensia

A

IgM normal, IgG normal or low, IgA and IgE decreAsEd

137
Q

radioallergosorbent assay = RAST

A

laboratory procedure that is designed to measure specific antibodies against given antigens (allergens). Usually looks at IgE specific for common allergens

138
Q

skin test

A

Test for allergies; Skin test is viewed as better for the correlation of allergies.

139
Q

mast cell degranulation is assoc with what kind of T cell response

A

TH2

140
Q

chronic ashthma is assoc with what kind of T cell response

A

TH2

141
Q

Derp1

A

cleaves occludin; primes TH2 response

142
Q

most allergens are proteins and many function as ___ which break intercellular junctions and allow the penetration of the allergens to the mucosal surface

A

proteases

143
Q

SPINK5 gene

A

codes for LEKT1 which usually inhibits serine peptidase

mutated in netherton syndrome

144
Q

clinical manifestations of Netherton syndrome

A

erythroderma (generalized skin erythema, pruritus, scaling of the skin, shivering, fatigue and fever)
atopic eczema
hair abnormality

145
Q

Netherton syndrome

A

mutation in SPINK5 gene causes LEKT1 inhibition of serine processes to be released (“inhibition of inhibition”) therefore serine peptidase destroy lots

Block 6: Immunology and Inflammation (6 decks)

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