Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

immuno final > part 1 review > Flashcards

part 1 review Flashcards

1
Q

B cells are attracted to follicles by:

A

CXCR5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

T cells are attracted to paracortex by:

A

CCR7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

PAMPs assoc with-

DAMPs assoc with-

A

PAMPs- micobes

DAMPs- damaged/necrotic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

typically, extracellular TLRs recognize ____ and intracellular recognize ___, exception?

A

extracellular- bacterial
intracellular- viral
exception- TLR9 is present in endosomes, recognized CpG DNA which is bacterial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

2 things that are activated by TLRs

A
  • NFkB = acute inflammation/adaptive immunity

- interferon reg factors=IFN a/b (antiviral defense)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

NOD-like receptors are present in the ____ and form ____ upon activation

A

cytosol; inflammasome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the action of NLRP-3?

A

cleaves Pro-IL-1B to IL-1B = inflammation and acute fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the exception in NLRs?

A

NOD2 is specific for bacterial peptides and does not trigger formation of inflammasome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

gd T cells

A

lymphs with limited diversity, recognize microbial lipids in CD1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

neutrophil production in bone marrow is stimulated by-

A

GM-CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

M1- formed by, actions

A

formation via signaling from TLRs and IFNg

promote inflammation, phagocytose/kill bacteria and fungi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

M2- formed by, actions

A

formation via signaling from IL-13, 14

release IL-10, TGFb and promote anti-inflam and wound healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

2 main functions of NK cells

A
  • kill virus infected cells by ADCC

- secrete IFNg to activate M1s to kill phagocytksed microbes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is NKG2D?

A

activating receptor on NK cell that recognizes MHC-I proteins expressed during cell stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is CD16?

A

activating receptor on NK cell that recognizes IgG on cell surface and kills cell via ADCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

responsible for the development and maturation of NK cells

A

IL-15

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

stimulates NK cells to release IFNg

A

IL-12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

NK T cells

A

in epithelia and lymph organs, recognize microbial lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

B1 cells

A

in peritoneal cavity and mucosa, produce IgM specific to microbial cell wall - “natural antibodies”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

marginal zone B cells

A

present in lymph follicle border, produce rapid antibody response against polysaccharide rice microbes in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

CRP targets ___ on microbe surface

A

phosphorylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how does CRP help fight infection? (2)

A
  • activates complement via classical pathway

- targets microbe for phagocytosis by macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

movement of WBCs into tissues is mediated by:

A

first selectins (weak) then integrins (stronger)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

antiviral defense substances

A

type 1 IFN (a/b) and NK cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what triggers the production of IFNs by virus-infected cells?

A

activation of TLRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

IL-10

A

anti-inflammatory, inhibits M1 activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

main “player” in mucosal immunity

A

MALT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

effect of commensals on paneth cells

A

commensals will regulate the composition of antimicrobial peptides released from paneth cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

why are commensals not eliminated from the intestine?

A
  • IECs express low levels of TLR 2, 4

- IECs express high levels of tollip (inhibitory)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

effect of commensals on dendritic cells

A

commensals result in immature DCs that will only given eek costimulatory signals in the LN and lead to the formation of Tregs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

effect of commensals on NFkB

A

commensals will block NFKB from binding to promoter through PPARg and IKB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

how do paneth cells “sense” microbes?

A

via TLRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what cells regulate paneth cells?

A

NK T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

2 genetic programs that are responsible for the antimicrobial peptides of paneth cells

A

MyD88 and NOD2-dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

IEL locations

A

CD8- closer to surface

CD4- in lamina propria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

“type a” activity of IELs

A

virus infected cell presents on MHC-I

IEL kills with perforin/granzyme and Fas-dependent path

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

“type b” activity of IELs

A

stressed cells express MIC-A and MIC-B
IELs bind MIC via NKG2D
kill via perforin/granzyme path

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

M cells are:

A

conduits for antigen sampling; targeted by some pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

FcRn dependent transport =

A

IgA binds antigen and carries across cell via FcRn to DC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

apoptosis dependent transport=

A

IEC undergoes apoptosis and fragments released to DC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

antigen capture=

A

DC squeezes between 2 IECs to grab antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

2 types of IgA

A

IgA1- planar, proteins

IgA2- kinked, LPS/carbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

functions of secretory IgA (2)

A
  • bind and neutralize pathogens or toxins in gut lumen or inside endosomes
  • export toxins/pathogens from the lamina propria into gut lumen for excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what will compensate in the case of SIgAD?

A

IgM will compensate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is released by DCs in mesenteric LN to trigger formation of Tregs?

A

IL-10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

oral tolerance is induced only by

A

mesenteric LN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is MHC restriction?

A

T cells can only recognize peptides when they are displayed on MHC molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

plasmacytoid DCs are directed against-

A

viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

genes for MHC-I

A

HLA-A,B,C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

structure of MHC-I

A

binding cleft made of a1/a2, conserved b2 region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

which cells express MHC-I?

A

all nucleated cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

how are antigens processed for presentation by MHC-I?

A

degraded in proteasome to fragments

fragments then pumped into ER by TAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

genes for MHC-II

A

HLA-DQ, DP, DR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

structure of MHC-II

A

binding cleft made of a1 and b1 subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

MHC-II expressed on:

A

dendritic cells, macrophages, B cells only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

how are antigens processed for presentation by MHC-II?

A

taken into cell by endocytosis, broken into fragments by proteases, ER produces MHC-II+CLIP and releases in vesicle, vesicles fuse, HLA-DM removes CLIP to leave IL and peptide binds MHC-II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

codominant expression of MHC genes increases-

polymorphism of MHC genes increases-

A

individual survival

population survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what causes bare lymphocyte syndrome?

A

MHC molecules do not form stably due to mutations in TAP or CLIP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

B cell antigen recognition differ from T cells: (4)

A
  • not limited to peptides
  • uses antibodies
  • no processing of antigen needed
  • antigens presented by FDCs or complement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

describe a thymocyte

A 
double positive (CD4, CD8)
expressing novel TCR ab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

thymocytes interact with ____ in the thymic ____

A

thymic epithelial cells

cortex

62
Q

end result of T cell maturation in thymus=

A

mature, naive T cells

63
Q

what will ingest the thymocytes that undergo apoptosis?

A

thymic macrophages (tingible macrophages)

64
Q

peptides used in T cell selection process are:

A

self peptides

65
Q

structure of TCR

A

1 a chain, 1 b chain

each chain with variable region (3CDRs) and constant region (anchors to membrane)

66
Q

TCR lacks

A

effector functions

67
Q

combinatorial diversity

A

different VDJ combinations

68
Q

junctional diversity

A

inaccurate gene splicing results in random insertion or cleavage of nucleotides

69
Q

Erk kinase

A

Erk kinase signaling influences development of gd T cells
strong Erk = gd T cell forms
weka Erk= ab T cell forms

70
Q

TNF family is located-

A

in the middle of MHC thus alteration in MHC = alteration in TNF

71
Q

2 states of Lck

A

inactive- phosphorylated

active- unphosphorylated, reveals kinase domain

72
Q

T cell structures involved in signal transduction

A

CD3, zeta

73
Q

T cell costimulator interaction

A

CD28 (t cell)

C7-1/B7-2 (activating cell)

74
Q

action of CD45

A

phosphatase that dephosphorylates/activated Lck

75
Q

where does ZAP70 bind?

A

double phosphate docking sites present on CD3 and zeta

76
Q

what are the actions of active ZAP70?

A

phosphorylation and activation of PLC, Ras/Rac, Pl-3 kinase = up regulation of transcription factor and protein synthesis

77
Q

what TFs are increased via T cell activation?

A

NFAT, NKkB, AP-1 (jun, fos)

78
Q

why is IL-2 important?

A

regulates clonal expansion of T cells

79
Q

effect of rapamycin

A

blocks IL-2R

80
Q

x-linked SCID caused by

A

mutation in Yc chain of IL-2R - causes failure to recruit JAK3

81
Q

what is CD25?

A

CD25 = IL-2Ra = high affinity

82
Q

what is the first molecule to be up regulated on the T cell surface following activation?

A

CD69

83
Q

how do cyclosporin/tacrolimus cause immune suppression?

A

PLC will increase calcineurin levels in cell

calcineurin inhibitors= NFAT remains phosphorylated and is unable to move into nucleus

84
Q

CD40L is expressed by:

A

CD4 T cells

85
Q

CD40/CD40L is the second signal for (3)

A

macrophages- phagocytosis, cytokine expression
B cells- isotope switching
Dendritic cells- costimulation, cytokine expression

86
Q

3 ways that CD8 T cell can kill a cell

A

initiate apoptosis via:

  • perforin/granzyme
  • fas/fas ligand
  • produce IFNg/TNK to activate NFKB = NO production
87
Q

mediators of migration of naive T cells through HEVs (3)

A

L-selectin, LFA-1 and CCR7

88
Q

present in efferent lymph vessel to lead T site to infection

A

S1P (that attracts S1PR1 on T cell surface)

89
Q

resistance of mycobacteria to cell mediated immunity=

A

inhibits phagolysosome

90
Q

resistance of HSV to cell mediated immunity=

A

interferes with TAP

91
Q

resistance of CMV to cell mediated immunity=

A

interferes with proteasome

92
Q

resistance of EBV to cell mediated immunity=

A

interferes with proteasome, secreted IL1-0 to block M1 activation

93
Q

resistance of Pox virus to cell mediated immunity=

A

secretes soluble receptors to IL-1 and IFNg to block their actions

94
Q

b cells use ___ for signal transduction

A

Iga and Igb

95
Q

affinity of B cells vs. T cells for antigen

A

B cells have a higher affinity and can also INCREASE their affinity as part of the maturation process

96
Q

most abundant Ig

A

IgG

97
Q

type of cell that dictates B cell selection

A

bone marrow stromal cells

98
Q

expressed by naive, mature B cells

A

IgM and IgD

99
Q

how are plasmacytes formed?

A

naive mature B cells interact with antigens on their surface, endocytose the antigen, process it and express it on MHC-II; CD4 T cell binds MHC-II and secretes cytokines to active B cell = plasmacyte that travels to germinal center of LN

100
Q

what attracts B cells to LN

A

SLC and MIP3B from dendritic cells

101
Q

what attracts B cells to follicles

A

BLC from FDCs

102
Q

what is somatic hypermutation?

A

b cell editing that yields daughter cells with varied affinity for antigen, daughter cells will interact with FDC and only those with high affinity will survive

103
Q

what enzymes are used in somatic hypermutation?

A

cytodine deaminase

uracil glycosylase

104
Q

what is isotope switching?

A

changing type of antibody from changes to Fc region

105
Q

what enzymes are used in isotope switching?

A

cytodine deaminase, uracil glycosylase, APE1

106
Q

what is meant by “thymus dependent”?

A

thymus dependent antigens are those that require T cell activation- peptide antigens are thymus dependent

107
Q

what signals class switching to IgG?

A

IFNg

108
Q

what signals class switching to IgE?

A

IL-4

109
Q

what signals class switching to IgA?

A

TGF-b and IL-10

110
Q

which Ig crosses placenta?

A

IgG

111
Q

which Ig activate complement?

A

IgM>IgG

112
Q

functions of IgG (6)

A
  • neutralization
  • opsonization
  • activate complement (classical)
  • activate NK cells for ADCC
  • neonatal Ig transfer
  • feedback inhibition of B cell activation
113
Q

function of IgM

A

-activate complement via classical pathway

114
Q

functions of IgA (2)

A
  • mucosal immunity

- neutralization

115
Q

functions of IgE (2)

A
  • granulocyte degranulation

- defense against helminths

116
Q

what helps to increase the half-life of IgG?

A

FcRn by protecting IgG from catabolism

117
Q

what is “opsonization”?

A

IgG coats the outside of microbe, then IgG binds to FcgRI or FcgRIIA on phagocytes and microbe is phagocytosed and killed

118
Q

what are the clinical implications of splenectomy?

A

spleen is reservoir for macrophages, thus if spleen is removed, pt is at risk for bacterial infections (encapsulated)

119
Q

FcgRI and FcgRIIA

A

located on phagocytes for phagocytosis of opsonized microbes

120
Q

FcgRIIB

A

for feedback inhibition of B cells and attenuation of inflammation

121
Q

FcgRIII

A

on NK cells for ADCC activation

122
Q

FceRI

A

on granulocytes, binding will signal degranulation

123
Q

alternative pathway C3 convertase

A

C3b+Bb

124
Q

alternative pathway C5 convertase

A

C3b+Bb+C3b+C5

125
Q

function on C3b, C4b on microbes

A

acts as opsonin (signals IgG to bind)

126
Q

functions of C5a, C3a, C4a

A

trigger inflammation

127
Q

initiator of classical pathway

A

C1 binds to antibody on microbe surface

128
Q

initiator of lectin pathway

A

mannose-binding lectin binds mannose on microbe surface

129
Q

C3 convertase in classical and lectin pathways

A

C4b+2a

130
Q

C5 convertase in classical and lectin pathways

A

C4b+2a+C3b+C5

131
Q

what triggers the late stages of complement cascade?

A

C5b

132
Q

properdin

A

stabilizes C3 convertase in alternative pathway

133
Q

3 end actions of the complement cascade

A

1-opsonization (C3b)
2- cytolysis via MAC formation (late steps triggered by C5b)
3- inflammation (C5a, C3a, C4a)

134
Q

DAF

A

decay accelerating factor

inactivates C3 convertase in alt pathway by displacing Bb

135
Q

MCP

A

prevents assembly of C1 to block activation via classical pathway

136
Q

C1 inhibitor

A

blocks protolytic activity of C1 (inhibits classical and MBL pathways)

137
Q

patients deficient in C1, C2 or C4 have increased risk to develop-

A

SLE

138
Q

complement def that is typically fatal in early life

A

C3

139
Q

def in C9 or MAC = increased susceptibility to

A

neisserial infections

140
Q

paroxysmal nocturnal hemoglobinuria

A

RBCs lack DAF and CD59 = susceptible to complement mediated attack/lysis, treat with anti-C5 antibody

141
Q

hereditary angioedema

A

def in C1 inhibitor causing accumulation of kallikrien/bradykinin, not “really” complement mediated disease

142
Q

C50 test will gauge

A

amount of serum required to lyse 50% of RBCs

increased C50 = decreased complement activity

143
Q

what surface markers are expressed by Tregs? transcription factors?

A

surface- CD4, CD25, CTLA-4

TF- FoxP3

144
Q

mutation in FoxP3 will cause

A

IPEX (deficiency of Tregs)

145
Q

what is AIRE?

A

present in thymic medullary cells, allows for expression of distant-tissue specific proteins

146
Q

absence of AIRE causes

A

APECED (autoimmune polyendocrine syndrome)

147
Q

clinical manifestations of autoimmunity depend on

A

antigen targeted

148
Q

NOD2 contributes to

A

crohn’s disease

149
Q

HLA-B27 is assoc with

A

ankylosing spondylitis (90%)

150
Q

what is the molecular mimicry hypothesis?

A

autoimmune diseases develop after exposure to antigen that is very similar to self

immuno final (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions