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Block 6: Immuno > Week 3 & 4 > Flashcards

Week 3 & 4 Flashcards

1
Q

CD16+

A

NK cells

peak response 3-4 days; no immunologic memory

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2
Q

congenital agranulocytosis

A

phagocytic deficiency

  • complete absence of neutrophils
  • ↓ production of G-CSF (acitvation of CTL)
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3
Q

leukocyte adhesion deficiency

A

phagocytic deficiency

  • leukocytes can’t extravasate/bad cell-cell interactions
  • lack β chain common to integrins (or selectin)
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4
Q

TH1

signal to activate, TF, what it secretes

A

signal: IL-12, IFNγ

TF: T-bet

secretes: IFNγ, IL-2

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5
Q

sjogren’s syndrome

A

autoantibodies and autoreactive T cells to ribonucleoprotein Ags → lymphocyte infilitration in exocrine glands leading to dry eyes and mouth

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6
Q

TLR4

A

recognizes LPS from gram negative bacteria

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7
Q

chronic rejection of kidney

A
  • glomerulitis: inflammation cells in capillary loop/accumulation of mesangial matrix
  • interstitial fibrosis and tubular atrophy
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8
Q

bare lymphocyte syndrome

A

combined immunity deficiency

  • dec. expression MHC I or II
  • all Ig decreased
  • defect in transcription of MHC genes; fatal w/o transplant
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9
Q

Belatacept

A

CTLA4:Fc fusion portein that binds to B7 to prevent the generation of signal 2 from CD28 to turn off T cell activation

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10
Q

tumor infiltrating lymphocytes (TIL)

A

isolated from solic tumors and activated with high doses IL-2; consists of CTL

re-injection is beneficial

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11
Q

cross presentation in cDCs

A

DCs take up viral Ags from outside the cell by phagocytosis of apoptotic cells (cells that die due to viral infection) and present on MHC I to CD8+

(normally foreign Ags are stim. MHC II and CD4+ but this way it stim. CTLs)

*important in acute transplant rejection

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12
Q

SCID mice

A

mutation in DNA protein kinase and deletion of recombination activating enzymes

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13
Q

CD40/CD40L

A

activates CD8+ CTLs to give help to B cells for Ab formation

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14
Q

chronic rejection

A

months-year post tranplanatation due to repetitive complement mediated cell damage and then vasculopathy (capillaropathy) with tissue injury, fibrosis and loss of function of graft

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15
Q

self-non self model of immunity

A

dendritic cells are activated thru triggering their PRR thru PAMPs that are essential for bacteria/not expressed by host

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16
Q

chronic rejection of heart

A

characterized by cardiac allograft vasculopathy (CAV) due to arteriole thickening and interstitial fibrosis; immunosuppressive drugs can’t treat

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17
Q

CCR5

A

cDCs express when they need to go to peripheral tissues and be resident there, then start upregulating CCR7

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18
Q

what signals activate the innate immune system, and what are the receptors that are activated?

A

PAMPs and DAMPs activate the innate immune system

they stimulate PRRs on phagocytes (granulocytes, macrophages, dendritic cells)

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19
Q

molecular mimicry

A

exposure of an Ag thatis very similar to self-Ag and induces immune response to infectious Ag and self Ag (ex. rheumatic fever in strep pyogenes)

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20
Q

multiple sclerosis

A

autoreactive T cells to brain antigens to MBP and MOG → sclerotic plaques and myelin destruction

T cell pathogenic; TH1 and TH17

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21
Q

GM-CSF

A

boosts Ag recognition phase: ↑ dendritic cells → CTL activation → tumor destruction

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22
Q

cross-matching

A

done to ID preformed anti-HLA Abs (for hyperacute rejection)

calcularte the PRA panel reactive antibody profile using:

  1. complement dependent cytotoxicity (CDC) assays
  2. flow cytometric crossmatch
  3. solid-phase assays (SPAs)
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23
Q

type I diabetes

A

autoreactive T cells to pancreatic islet cell Ags → destruction of β cells leading to non-production of insulin

T cell pathogenic

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24
Q

myasthenia gravis

A

auto antibodies to Ach R on SkM (B cell pathogenic) leading to inhibition of SkM contraction and weakness

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25
Q

dose-response relationship

A

monotopic (unidirectional) response curve; ex. amount of smoking and lung cancer

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26
Q

strength of the association

A

stronger association is more likely to be causal; weaker association is more likely to be explained by undetected bias

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27
Q

dendritic cell cycle

A

live in resting state in peropheral tissues → activated and go thru afferent lymphatic vessel to node and present Ag → T cells clonally expand → T cells leave lymph node for site of inflammation

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28
Q

graft vs. host disease

A

life threatening complication of HSCT whereit attacks normal tissue (skin, intestine, liver, lung) and reconstitutes thymocytes/hematopoetic cells. caused by infused donor T cells including CD4+ and CD8+; assoc. with ↓ risk of leukemic relapse

minor histocompatability also contributes - caused by HY antigens in M but not F (if sister is receiving from brother, T cells specific for self antigens are on brothers cells but not same HLA as sister). most miHLAs are presented by MHC I

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29
Q

tumor specific antigen (TSA)

A

not expressed on normal cells and are unique to tumor cells:

  1. mutation in gene that is in normal cells (K-ras)
  2. protein in tumor cells but not normal cells (viral protein)
  3. unusual mRNA splicing/post-translational modification
  4. hybrid/chimeric protein from chromosomal translocation
    1. makes new epitope
    2. CML/phila chromosome (9:22) Bcr/Abl is oncoprotein
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30
Q

CAR T therapy

A

T cell collection for B cell lymphoma → express CD19 sepecific Ig linked to CD3 → put back in patient

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31
Q

TLR5

A

binds flagellated bacteria

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32
Q

Treg

signal to activate, TF, what it secretes

A

signal to activate: TGFβ

TF: foxp3

secretes: TGFβ, IL-10

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33
Q

cDC vs pDC markers

A

cDC: express MHC I and II (MHC II is expressed intracellular until triggerred by PRR), also upregulate ICAM1, LFA1 and B7 (CD80/86)

pDC: IFNα and β, express TLR7 and TLR9 to sense viral nucleic acids. make 1000x more IFNs than any other blood cell type

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34
Q

immune system activation (normal and when rejecting a graft) 3 steps:

A
  1. Ag + MHC recognition
    1. MHC I has 3 domains and peptide binding is between α1 and α2 - present to CD8+
    2. MHC II is α and β chain - present to CD4+ processed in endocytic compartment
  2. costimulatory molecules
  3. pro-inflammatory cytokines
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35
Q

x-linked bruton’s agammaglobulinemia

A

humoral immunity deficiency

  • lack of mature B cells
  • all Ig classes ↓
  • due to defect in bruton’s tyrosine kinase for B cell development
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36
Q

humoral immunity deficiencies

A
  • recurrent infections
  • lack of long term protection/antiviral immunity
  • delay of onset due to passive transfer of maternal IgG
  • tx with passive admin of normal Igs
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37
Q

lymphokine associated killers LAK

A

obtained from acitvation of peripheral blood mononuclear cells of cancer patients with high IL-2

consists of NK cells; reinjection is beneficial but activity per cell isn’t as good as TIL

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38
Q

acute rejection:

how long does it take

A

2 weeks to 3 months due to requiring time to activate and clonally expand B and T cells; 2nd reaction is due to memory T cells

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39
Q

peripheral tolerance

A

unresponsiveness induced in mature lymphocytes that have recognized their Ag → lack of signal 3 (cytokines) → anergy

tolerogenic APC tolerizes CD4+ cells; failuret o activate Th leads to B cell energy and lack of CTL

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40
Q

monogenic autoimmuntiy

A

immunity assoc. with one gene

  • AIRE - APS-1
  • CTLA4 - graves, TID
  • FOXP3 - IPEX
  • FAS - ALPS
  • C1q - SLE
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41
Q

minor histocompatability ex.

A

HY in mice is encoded on Y chromosome/only expressed in males so females reject it; different in humans because we are so polymorphic

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42
Q

atacxia-telangiectasia

A

immunodeficiencies assoc. with other defects

  • abnormal walk, vascular malformations
  • ↓ IgA and IgE, IgM normal, IgG normal/decreased, T cells ↓
  • malignancy prone
  • ATM gene mutation (protein in DNA repair)
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43
Q

TH2

signal to activate, TF, what it secretes

A

signal: IL-4

TF: GATA3

secretes: IL-4, IL-5

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44
Q

main target of hyperacute rejection

A

vascular endothelium

(in kidneys leads to dec. RA perfusion secondary to vascular spasm, microvascular injury/intravascular coagulation)

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45
Q

selective IgA deficiency

A

humoral immunity deficiency

  • most common immunodef.
  • respiratory and GI infections
  • (can’t treat with Igs because not enough for lack of secretory IgA)
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46
Q

acute rejection of heart: cell mediated vs humoral

A

cell mediated: maybe reversible with subtle enlargement/ECG changes and ↓ EF, interstitial infiltrate

humoral: high death rate, no infilitrate, due to endothelial swelling - can see Igs on surface thru immunofluoresence

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47
Q

hashimoto’s thyroiditis

A

autoantibodies and autoreactive T cells to thyroid Ags → hypothyroidism thru destruction of tissue

Th1 mediated; causes DTH

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48
Q

antibody mediated rejection AMR

tx?

A

activation of B cells to produce Abs (seen in indirect recognition of allo-Ag). due to:

  1. undetected preformed memory response
  2. newly acute primary response
  3. fixing complement onto BVs (deposits on capillary endothelium)

tx: rituximab, Ab that binds CD20, GCs, IV IG

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49
Q

selective IgG subclass deficiency

A

humoral immunity deficiency

  • decrease in IgG2 or IgG3 (but total IgG levels normal)
  • asymptomatic
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50
Q

5 susceptible genes leading to autoimmune disease

A
  1. HLA alleles
  2. genes in clearance of apoptocic cells
  3. genes in TCR BCR signaling
  4. genes in negative regulation of lymphocyte activation
  5. genes in lymphocyte apoptosis
51
Q

TH17

signal to activate, TF, what it secretes

A

signal to activate: TGFβ and IL-6

TF: RORγT

secretes: IL-6, IL-17

52
Q

migratory DCs

A

CD14+ dendritic cells secrete IL-12 which activates Tfh leading to plasma cells and long lived memory B cells

ex. langerhans cells of epidermis and interstitial DCs of dermis; sample Ag in peripheral tissues and then migrate to Lymph nodes where they present to CD4+ and Tfh

good at cross presentation to CD8+ to present to MHC I

53
Q

acute rejection in kidney

A

capillaritis; inflammation in peritubular capillaries and complement deposition C4d in peritubular capillaries and glomerulus

54
Q

x-linked hyper-IgM syndrome

A

humoral immunity deficiency

  • dec. IgA and IgG, increased IgM
  • mutation in CD40L; can’t interact for B cell activation
  • inhibition of B cell response to T dependent Ags
55
Q

TH1 secretes what which does what

A

IL-2 which interacts with IL-2 R on naive CTL to boost/make more CTL to kill tumor cells

(dont forget Th1 is CD4 so it interacts with MHC II, and CTL is CD8 so it interacts with MHC I)

56
Q

digeorge syndrome

A

cellular immunity deficiency

  • lack thymus, parathyroid glands
  • CVD and facial abnormalities
  • T cell count and functions ↓ but increase w/ age (ectopic thymus)
  • microdeletions on chromosome 22
  • humoral immunity also affected
57
Q

PD-1

A

binds SHP1-2 phosphatases and reduces signaling of TCR → dec. T cell prolif, survival and IL-2 production

58
Q

plasmacytoid DCs

A

CD123 BDCA-2+

secrete type I IFNs “interfere” with viral replication; mostly make IFNα

59
Q

chronic granulomatous disease

A

phagocytic deficiency

  • x-linked, most common
  • defect in cytochrome b needed for peroxide production
  • bacteria get injested but aren’t killed / get transported to organs
  • tx: give recombinant IFNγ
60
Q

SLE

A

autoantibodies and autoreactive T cells against DNA, chromatin proteins, and ribonucleoprotein antigens → glomerulonephritis, vasculitis, rash

B cell pathogenic, type III hypersensitivity (proliferative glomerulitis and vasculitis) but disease if disordered immunity

61
Q

direct vs. indirect recognition of allo-Ag

A

direct: APCs from graft mgrate out and go to draining lymph node, get recognized by host T cells (CD4 help CD8 become CTL) thru recognition of donor MHC and foreign peptide

indirect: host APCs get to graft, aquire donor specific Ags and go to lymph nodes/present to T cells which recognize self MHC and donor Ag; cross presentation important where dendritic cells present on MHC I to CD8 - important in graft rejection after donor DCs die in 1st days post transplantation. Self MHC CD4 cells secrete IL-2, IL-4, IL-5 (eosinophilic infiltration), IFNγ (act. macrophages) to facilitate DTH (macrophage activation) and activation of B cells to produce antibodies (AMR antibody mediated rejection)

62
Q

multistep process of tumor formation:

A

loss of APC → hyperproliferative epithelium

DNA hypomethylation → early adenoma (benign)

activation of K-ras → intermediate adenoma

loss of DCC → late adenoma

loss of p53 → carcinoma → metastatis

63
Q

TLR2,4,6

A

recognize products of oxidative stress (oxidized LDLs/phospholopids) and molecules released by dying cells like HMGB1

64
Q

CD45-44

A

maintain engaged the APC-Tcell interaction

65
Q

acute rejection in liver

A

reversible cell mediated rejection

diagnostic triad: portal inflammatory infiltrate, bile duct damage, endothelitis - lymphocytes, eosinophils

use Banff grading for liver rejection

66
Q

adaptive t regs

A
  1. deletional tolerance (recessive) - self reative T cells deleted in thymus; can be activatd in perophery
  2. regulatory tolerance (dominant)/infectious tolerance - T cells specific for self Ag become Treg; regulatory DCs make TGF β and IL-10; require TGFβ and IL-2 to survive and express CD25
67
Q

hyperacute rejection

what type of hypersensitivity is it?

prevention?

why are xenografts so immunogenic?

A

within hours due to Abs from previous exposure to Allo-Ag (multiple pregnancies, blood transfusions) or ABO mismatch

activates complement → thrombosis and hemorrhage and neutrophil invasion

type II hypersensitivity (Ags present on cell surgcae leads to complement activation)

prevent with plasmapheresis and IVIG

xenografts so immunogenic because CD59 and DAF are less effective at complement inhibition

68
Q

what 2 signals do B cells need to activate?

A
  1. binding of Ag to BCR
  2. CD40/CD40L on CD4+ Tfh cells → B cell proliferation, isotype switch and Ab production

*anergy without this

69
Q

rapamycin

A

blocks response of T cells to IL-2

downstream of IL-2 is mTOR that leads to AKT activation for cell survival and proliferation

70
Q

TLRs 3, 7, 8, 9

A

recognize nucleic acids after their shuttled to endosomal compartments of APCs via endocytosis and phagocytosis

TLR3: dsRNA

TLR7,8: ssRNA
TLR9: CPGs that come from viruses

71
Q

rheumatoid arthritis

rheumatoid factor

A

autoreactive T cells to antigens of joint synovium

CD4+ fells make TNFα and IL-6 which activates fibroblast like synoviocute cells to make MMPs (cartilage damage) and RANKL (bone erosion)

rheumatoid factor: an auto-Ab (IgM) that recognizes Fc portion of IgG

autoantibodies to citrullinated peptides (Arg → cit by PAD peptidyl arginine deaminase) which are presented to CD4 cells, trigger complement

72
Q

Tfh

signal to activate, TF, what it secretes

A

signal to activate: IL-6

TF: Bcl6

secretes: IL-21, ICOS

73
Q

specificity of the association

A

an invalid criterion - smoking has multiple effects

74
Q

resident DC

A

in lymphoid tissue; acquire and present Ags within lymphoid organs

75
Q

wiskott-aldrick syndrome

A

immunodeficiencies assoc. with other defects

  • thrombocytopenia, eczema, bacterial infections
  • IgM ↓, IgA and IgE ↑, IgG normal
  • defective response to bacterial polysaccharides
  • x-linked defect in WASP gene that encodes protein for signal transduction/cytoskeleton of T cells
76
Q

central tolerance

A

eliminating autoreactive T and B cells during development in central lymphoid organs, thymus and BM where self-Ags are expressed for induction of tolerance

  1. apoptosis (deletion in b and t cells)
  2. anergy (b cells)
  3. changes in B cell receptors / RAG reactivation
  4. development of Treg
77
Q

Danger model of immunity

A

dendritic cells are activated by endogenous stress signals thru DAMPs recognized by PRRs

78
Q

2 things that label cell and self/don’t kill by NK cell

A 
class I MHC
AR ligand (AR is on NK cell)

if MHC I downregulated, in virus/cancer cell, NK cell will kill

79
Q

heteroconjugate of anti-CD3 and anti-TSA/TAA

A

facilitates T cell immune repsonse to tumor cells by bringing T cells and cancer cells close together

80
Q

common variable immunodeficiency

A

humoral immunity deficiency

  • B cells don’t mature into plasma cells
  • ↓ in Ab producing plasma cells
  • ↓ all Ig classes
  • recurrent infections
81
Q

CCR7

A

allows DCs to move to the draining lymph node through lymph and end up in T cell area to present to T cells, also upregulates MHC expression I and II

82
Q

ICOS

A

on surface of germinal T cells for Tfh/CD4+ required to help B cells; without it mice can’t Ab isotype switch. ICOS-L is expressed by activated APCs

83
Q

antimicrobial activity of macrophages

A
  1. O2 dependent: ROS, H2O2, and NO
  2. O2 independent: lysozyme, defensins
84
Q

Goodpasture’s syndrome

A

auto-Abs against basement membrane type IV collagen of glomerulus → glomerulonephritis

85
Q

immunological tolerance

A

unresponsiveness to an Ag due to previous encounter of specific lymphocytes with their Ag in conditions that inhibit their activation

required for life. failure = autoimmune disease

86
Q

cytokine escape strategy of tumor cells

A

they secrete TGFβ (inhibits Th1 cells) and IL-10 (inhibits macrophages)

87
Q

CTLA-4

A

inhibits T cell activation by:

  1. stimulating phosphatases SHP-1 tht inhibit TCR
  2. competes with CD28 for binding (and is 20x more avid)

Abs to block CTLA4 in tumor treatment to get the T cells to attack tumor

88
Q

CD28

A

costimulatory molecule in Ig superfamily that binds CD80/86 (B7) which induces T cell proliferation and NFAT regulated IL-2 production and T cell survival, enhances NFKB translocation to nucleus which activates pro-survival genes (Bcl-xl)

89
Q

graves disease

A

autoantibodies to TSH R → hyperthyroidism

90
Q

tissue typing

A

PCR to determine HLA of donor and recipient to see how different their haplotypes are (DNA test) - T cells from recipient are incubated with donor cells and cytotoxicity is measured

91
Q

tumor associated antigen (TAA)

A

not unique to tumor cells - expressed in low levels in normal cells/fetal cells:

  1. c-myc: constitutive overexpression → HER2 breast cancer
    1. Burkitt’s lymphoma
  2. α fetoprotein AFP and carcinoembryonic ag CEA: on fetal cells
    1. AFP high in liver cancer
    2. CEA high in pancreatic and colorectal cancer
92
Q

SCID

A

combined immunodeficiency

  • fatal unless tx with BM transplant
  • lack B and T cells; all Ig low
  • causes:
    • x-linked coding for γ chain of IL-2 family (IL-2, IL-4, IL-7, IL-11, IL-15)
    • mutated JAK3 kinase (autosomal recessive)
    • defect in RAG1 or RAG2 - lack of rearrangement of TCR/Ig
    • adenosine deaminase ADA or purine nucleoside phosphorylase PNP deficiency - ADA is toxic metabolites for B and T cells, PNP is mostly B cells
93
Q

AIRE

A

autoimmune regulatory - allows ectopic expression in thymic medulla of peripheral tissues specific Ags so that they can be presented in the thymus and induce negative selection of thymocytes autoreactive for them

disorder = APS-1 where immune system attacks/destroys endocrine glands → hypothyroidism, hypoparathyroidism, addison’s disease, diabetes

94
Q

sources of hematopoetic stem cells

A
  1. BM HSC: from iliac crest
  2. PB HSC: recruit HSC from bone marrow into peripheral blood once treated with G-CSF and GM-CSF, the extract Abs with CD34
  3. umbilical cord blood: from placenta - have fewer alloreactive T cells
  4. spleen - but not lymph node
95
Q

temporality

A

exposure to factor must precede outcome - hard to demonstrate in diseases with long latent periods (london fog, food-bore illnesses)

96
Q

allo-antigen

A

molecules recognized as different by the immune system of members of the same species; MHC (series of genes clustered into a haplotype) are most important/cause alloreactivity

97
Q

3 types of APCs

A

dendritic cells, macrophages, B cells (but B cells only present one specific Ag because they don’t phagocytose)

98
Q

corticosteroids:

  1. mechanism of action
  2. indications
  3. adverse effects
A
  1. reduce size of lymph nodes/spleen and interfere with cell cycle of activated lymhoid cells; indirectly induce T cell death; suppress Ab/PG/leukotriene formation
    1. block monocyte production of cytokines like IL-1 for T cell maturation
  2. autoimmune, allergies, bronchial asthma, transplant
  3. weight gain, psychoses, glucose intolerance, HTN, cataracts, skin fragility, bone dissolution, infection, cushingoid reactions (moon face, weight gain, facial hair, acne, buffalo hump, weird skin)
99
Q

cyclosporine A

  1. mechanism of action
  2. indications
A
  1. selective inh. T cell activation - inh. IL-2; binds cyclophilin (FKBP) and inihibts calcineurin → NFAT not activated to nucleus → no IL-2 made
  2. inhibition of transplant reactions
100
Q

tacrolimus (FK506)

A

macrolide antibiotic from strep tsukubaenis

(like CsA) binds to FKBP and inhibits calcineurin → ↓ IL-2; blocks activation of T cells

more potent than CsA

indicated in trasplants

101
Q

rapamycin (sirolimus)

A

macrolide Ab like FK506

binds FKBP and inhibits IL-2R

reduced toxicity than CsA/FK506 but better in combination therapy

102
Q

thalidomide

A

useful in skin manifestations of lupus

103
Q

mycophenolate mofitil

A

inhibits de novo pathway of purine/pyrimidine synthesis

104
Q

azathioprine

  1. mechanism of action
  2. uses
A
  1. antimetabolite - interferes with NA metabolism. absorbed in GI and metabolized to mercaptourine; deactivated by xanthine oxidase before excretion
  2. combined with prednisone in transplants, glomerulonephritis/lupus, RA
105
Q

cyclophosphamide

A

alkylating agent - most potent immunosuppressive drug. converted to active in liver which can cross like DNA and inhibit RNA synthesis → destroys proliferating lymphoid cells and alkylates resting cells

use very large single dose

*NOT SELECTIVE

106
Q

methotrexate

A

folate antimetabolite; prophylaxis for GvHD/severe RA

major AE is infection/GI

107
Q

type I hypersensitivity treatment

A

IgE mediated releases assoc. with ↓ cAMP; treat by giving cAMP (catecholamines, corticosteroids, theophylline), chromolyn sodium prevents mast cell degranulation, antihistamines

108
Q

Rh incompatability is what type of hypersensitvity

A

type II

109
Q

formula of secretory IgA

A

(IgA)2JSC

heavier than serum IgA

110
Q

where can u find M cells

A

above peyer’s patches

111
Q

where does immune activity in gastric mucosa occur?

A

in the lamina propria

112
Q

production/transcytosis/secretion of IgA

A

plasma cell produces dimeric IgA in lamina propria → bind to poly-Ig receptor → receptor mediated endocytosis/transport to apical surface → receptor cleaved but SC stays on dimer

113
Q

5 functions of sIgA

A
  1. inhibition of microbial attachment @ mucosa
  2. neutralization of viruses/toxins @ mucosa
  3. containment of normal microbes in gut
  4. inh. absorption of undigested foreign Ags
  5. (colostrum) passively protects infant GI tract
114
Q

why do IgA deficient patients survive?

A

compensation by IgM and IgG

115
Q

IgA1 vs IgA2

A

IgA1: predominates in blood - many bacteria have IgA1 protease to invade - influenza, gonorrhea, meningitis, strep

IgA2: missing 13AA in hinge region; predominates in SI and vagina

116
Q

do peyers patches have afferent lymphatics?

A

NO!!!! M cells are pinocytotic and sample environment of GI tract

Ag is taken in by M cell, presented by DC which activates T cells

117
Q

where are inductive sites for production of IgA committed (switched) B cells?

A

peyers patches and ILFs (scattered isolated lymphoid follicles) and mesenteric lymph nodes

118
Q

how do B cells get to GI tract?

A

B cells have integrin α4β7 and chemokine receptor CCR9

gut epithelial cells have CCR9 ligand CCL25

capillary HEV express MadCAM1 which binds integrin α4β7

119
Q

whats the major switch factor for IgA

A

TGFβ

is T cell dependent/requires CD40; TFH drives IgA production once switching has occureed; IL-5 and IL-6 promot differentiation

120
Q

T-dependent sIgA response

A

B2 cells in peyers patch; co-stimulatory signals signals from DCs and Th2; drive switch from IgM to IgA; make lots of IgG

in secondary lymphoid organs

121
Q

T-independent sIgA response

A

B1 cells; occurs in ILFs; main response to commensal bacteria in gut

makes lots of IgM

in peritoneal and pleural cavitites

APRIL in B1 cell development

122
Q

IELs

A

located between epithelial cells, CD8+ with γdelta - contribute to host defense (cytotoxicity) and immunosuppressions and tolerance (makes TGFβ and IL-10)

123
Q

what type of T cells are in the LP and mesenteric lymph nodes?

A

CD4+ that help B cells by making IL-5 and IL-6

Tregs - mediate tolerance

124
Q

TGFβ paradox

A

both an immunosuppressive cytokine by Tregs and a switch factor for IgA synthesis

Block 6: Immuno (3 decks)

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