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Block 6: Immuno > Week 2 > Flashcards

Week 2 Flashcards

1
Q

clonal anergy

A

cell becomes non-responsive to complete phsyiological stimulation

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2
Q

Th1

A

activate macrophages

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3
Q

what type of receptors are monospecific and what does that mean

A

γδ are monospecific; entire wave has single TCR

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4
Q

positive thymic selection vs negative

A

positive: regcogize self MHC
negative: can’t be too self-reactive (can’t bind too tightly)

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5
Q

what are the 2 checkpoints for α:β T cells in the thymus?

A
  1. after rearrangement of β genes (then can become double negative then immature double positive)
  2. after rearrangement of α genes (then can become mature double positive cells)
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6
Q

what molecule is required for triggering NFKB?

A

CD28 and PKC theta

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7
Q

IL-6

A

acute phase proteins, neutrophils, fever

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8
Q

genetics of MHC I

A

codes for 20 genes but 3 of them (A, B, C) code for MHC I molecules that present to CD8 cells

have 1 set from each parent so 6 molecules total

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9
Q

where are TCR γδ?

A

primarily in tissues; don’t undergo thymic development/not in secondary lymphoid structures but in organ epithelium (short term defense?)

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10
Q

IFN γ

A

macrophage killing, MHC II expression, anti-viral response

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11
Q

serum sickness

A

type III hypersensitivity

using horse Abs against foreign pathogen

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12
Q

CD28

A

costimulatory molecule (binds to B7 on APC)

once TCR binds to Ag/MHC, CD28 is activated and drives T cells to differentated and stim. expression of CTLA-4 as negative feedback

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13
Q

ITAMs (immunorecognition tyr based activation motif)

A

binding of MHC to TCR → phosphorylation of ITAMs then zap70 binds to ITAMs and is activated by Lck

zap70 phosphorylates proteins which activates PLC γ which activates DAG (stays in PM) and IP3 (goes to cytosol to mobilize Ca)

activates TFs (NFAT, AP-1)

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14
Q

homeostatic proliferation

A

T cells in periphery proliferate/keep numbers constant even into age as thymic gland involutes

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15
Q

CTLA-4

A

co-inhibitory molecule (binds B7 on APC)

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16
Q

Treg

A

elicited by TGFβ, express FOXP3 TF

inhibit T and B and dendritic cells to down regulate immune response

FOXP3 responsible for IPEX (immunodysregulation, polyendocrinopathy, enteropathy, X linked syndrome)

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17
Q

naturally occurring blood antibodies are of what class

A

IgM

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18
Q

type III allergic reaction

A

IgG

activates complement/phagocytes

in serum sickness, arthus reaction

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19
Q

microbial superantigens

A

bind MHC II outside of peptide groove (no processing involved); bind multiple TCRs via β chain → cytokine storm

*level of T cells activated several logs greater than normal

can be produced by Staph or Strep (Staph is worse mortality) - thru tampon use, respiraotry airway infections, food poisoning

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20
Q

IL-2

A

drives clonal expansion and differentiation of naive T cells

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21
Q

sensitization

A
  • der p 1 (made by dust mites) degrades TJs
  • Ag gets taken up by dendritic cell
  • TH2 induces B cells to class switch to IgE
  • Abs against der p 1 are made
  • mast cell degranulates when encounters –> allergic symptoms

reason why 1st bee sting not bad but 2nd is

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22
Q

type I allergic reaction

A

IgE

mast cell activation

in allergic rhitinis/allergic asthma/atopic eczema/systemic anaphylaxis/some drug allergies

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23
Q

pre-TCR

A

β chain rearranges first then pairs with pTα which is surrogate; heterodimer binds to CD3 which signals to cell success

allows for:

  • α chain rearrangement
  • expression of CD4 and CD8
  • proliferation
  • stops additional β arrangements
  • shuts off pTα
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24
Q

IL-10

A

down regulates immune response

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25
Q

proteins of CTL

A
  • perforin: permeabilizes target cell
  • granzyme: serine proteases for activating apoptosis once inside
  • granulysin: antimicrobial actions, can induce apoptosis

also CTL express FasL and IFNγ (inc. recognition by MHC I and peptide transporter molecles) and TNFα

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26
Q

HEV

A

T cells go thru it in lymph node before they meet up w an APC

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27
Q

thymocyte

A

T cell in thymus; not activated there to generate imunne response; don’t recirculate

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28
Q

type IV allergic reaction

A

TH1: activates macrophages, in allergic contact dermatitis and TB reaction

TH2: IgE production/eosinophil activation, in chronic asthma/chronic allergic rhinitis

CTL: cytotoxicity, in graft rejection and allergic contact dermatitis to poison ivy

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29
Q

Tfh

A

activate B cells and Ab production in germinal centers

30
Q

expression of TCR/CD3 on the membrane depends on what?

A

zeta chain

31
Q

CD40-CD40L

A

for interactions between Ag presenting cells and T cells; Ab response (class switch and somatic mutations)

mutation results in X linked hyper IgM syndrome

32
Q

CAR T cell technology

A

harvest pt T cells (for B cell lymphoma)

add retrovirus that recognizes CD3/CD28 that encodes anti-CD19; put T cells back into patient

33
Q

anti-CD3 Ab or lectin

A

can cross link TCR/CD3 mimicking an Ag so cells are tricked into releasing Ca/DAG

34
Q

S1P

A

concentration higher in lymph than lymph nodes - T cells have S1PR1 so they can leave the lymph nodes, but CD69 forms complex with SIPR1 so T cells won’t leave if there’s an Ag present in lymph node

35
Q

TH2

A

help in antibody production

36
Q

H antigen

A

Backbone of ABO system (coded for by FUT1)

bombay phenotype if don’t have

37
Q

cyclosporin pathway

A

normally Ca binds to calmodulin then calcineurin binds to that

complex activates NFAt which goes to nucleus to transcribe IL-2

cyclosporin binds to an immunophilin which sequesters calcineurin

38
Q

ionophores

A

cyclical compounds that pick up/drop off Ca (chelate Ca)

ex. PMA mimicks DAG, exerts similar effects

39
Q

class I vs class II vs class III MHC

A
  • class I: on surface of all cells, bind/present to CD8 cells
  • class II: on APCs, bind/present to CD4 cells
  • class III: encode proteins involved in inflammation like complement and TNFα
40
Q

Th17

A

elicited by TGFβ and IL-6, express RORγT TF

recruit neutrophils during early bacterial/fungal infections - abnormal activation leads to autoimmunity

41
Q

classic hybridoma technology

A

to make MoAB

immunize animal with Ag, collect Ab, transfer to HAT medium, select hybridoma for right Ag and then clone

42
Q

MHC is so diverse because of

A

polymorphisms (many alleles in the population) and polygeny (several types of MHC molecules within 1 person)

43
Q

can TCR-CD3 alone complete the signal?

A

No! it is incomplete and causes anergy - need B7 CD28 to make naive T cell fully activated

44
Q

peptide processing in MHC II

A

acid proteases degrade extracellular proteins taken in by endocytosis

invariant chain (binds in groove of MHC II) processed to CLIP then those endosomes fuse and the complex is expressed on the cell surface

HLA-DM binds to MHC II releasing CLIP and allowing other peptides to bind/MHC can go to cell surface

45
Q

A vs B antigen (biochemically)

A

ABO locus codes for glycosyl transferase

A is N-acetylgalactosamine (A codes for N-acetylgalactosamine)

B is galactose (B codes for galactose transferase)

46
Q

peptide anchor residues

A

side chains of amino acid residues of the peptide fit into pockets of the peptide-binding cleft of the MHC

47
Q

dual role of TGFβ

A

activates both Treg and TH17 which do oppostite things

48
Q

IFNα/β

A

antiviral

49
Q

genetics of MHC II

A

2 genes encode α and β chains at 3 loci (DP, DQ, DR)

each individual inherits a molecule from each parent so 6 ottal BUT α chain from one gene can associate with β chain from another gene so 12 different molecules can be expressed (good because more possibilities of loading peptides)

50
Q

tissue transglutaminase (ttg)

A

modifies gluten peptides so they bind to MHC II activating T cells which secrete IFN gamma

gluten peptides also tell epithelial cells to express MIC then lymphocytes kill that epithelium

51
Q

peptide processing MHC I

A

proteasomes (complex of proteins that degrades into peptides along with self peptides) degrade endogenous proteins made by viruses/intracellular parasites

polyubiquitinated proteins are bound by 19S cap and degraded in catalytic core/proteins released into cytosol

partially folded MHC I α chains bind to calnexin then to chaperone proteins (calreticulin) then TAP (req. ATP) delivers peptides to ER; a peptide binds MHC I to complete its folding and MHC I is released from TAP/exported to cell membrane

52
Q

clonal deletion

A

only cells with TCR will die. the rest stay alive

53
Q

steps of leukocyte extravasation/molecules involved

A
  1. rolling: selectin/mucin
  2. activation: chemokine
  3. adhesin: integrin/CAM
  4. diapedesis: PECAM
54
Q

prolonged DTH response

A

granuloma formation

Th1 cells activate macrophages which harbor and kill intracellular bacteria

inject Ag intradermally and wait for response; positive skin reaction indicates sensitized Th1 cells showing that pt has been exposed to Ag previously

55
Q

digeorge syndrome

A

lack of thymus due to deletion of chromosome 22 - patient lacks mature T cells so can’t do B or T cell responses; also facial abnormalities and CVD

56
Q

makeup of MHC II protein

A

α and β chain both anchored to membrane/bound together non-covalently; coded for by different set of genes.

cleft in center binds peptide; formed by interaction between α1 and β1 to present to CD4 cells

57
Q

western blotting

A
  • take virus, dissociate with detergent
  • run on SDS PAGE
  • transfer to nitrocellulose paper and add antiserum
  • add anti-IgG
58
Q

Th17

A

promote IL-17 mediated inflammatory response

59
Q

makeup of MHC I protein

A

α chain (made of α1, α2, and α3)

β2 microglobulin - shorter chain bound noncovalently to α chain

each domain is 110 AA long with disulfide bonds

60
Q

TH2 leads to release of what cytokines

A

IL-4 (B cell activation)

IL-5 (eosinophils)

61
Q

IL-12

A

T cell differentiation (TH1)

62
Q

haplotype

A

each set of alleles encoding MHC inherited from a parent

(theres a 1/4 chance that 2 siblings will have identical haplotypes)

63
Q

Tc

A

kill tumor and virus infected cells, reject histoincompatible grafts

64
Q

hygeine theory

A

early exposure to ubiquitous microorganisms plus good genes can lead to non-atopic (no hypersensitivity reaction)

65
Q

what are the 5 classes of cytokine receptors are what are the ligands of each?

A
  1. Ig superfamily of receptors: ligands IL-1, M-CSF
  2. class I cytokine receptors:
    1. IL-2: T cell proliferation
    2. IL-6: acute phase proteins, fever
    3. IL-4: B cell activation (Th2)
    4. IL-12: T cell differentiation (Th1)
  3. class II cytokine receptors: ligands IFNα/β, IFNγ
  4. TNF receptors:
    1. TNFα/β: pro-inflammatory
    2. CD40: B cell activation
    3. Fas: apoptosis
  5. chemokine/GPCR - for cell recruitment during development/inflammation
66
Q

major vs minor cross match

A

major: donor RBCs + recipient serum
minor: donor serum + recipient RBCs

67
Q

TH1 leads to relase of what cytokines

A

IFNγ and IL-2 (T cell differentiation)

68
Q

delayed type hypersensitivity (type IV hypersensitivity)

A

DTH Ag → Th1 cells secrete cytokines → localized inflammatory reaction (macrophages)

2 phases:

  1. sensitizaiton/induction: T cell expansion/differentiation
  2. effector phase: make lots of IFNγ “armed macrophage”
69
Q

PECAM

A

binds to itself to mediate diapedesis

70
Q

IL-4

A

B cell activation (Th2)

71
Q

drug hypersensitivity and HLA alleles

A

abacavir binds in groove of HLA B*57:01 (MHC Class I) and changes peptide binding characteristics; presentation of novel self-peptides leads to T cell activation

72
Q

type II allergic reaction

A

IgG

Ag activates complement or receptor alters Ab signaling

involved in some drug allergies, chronic uticaria

Block 6: Immuno (3 decks)

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