Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Block 6: Immuno > Week 2 > Flashcards

Week 2 Flashcards

(72 cards)

Start Studying
1
Q

clonal anergy

A

cell becomes non-responsive to complete phsyiological stimulation

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

Th1

A

activate macrophages

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

what type of receptors are monospecific and what does that mean

A

γδ are monospecific; entire wave has single TCR

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

positive thymic selection vs negative

A

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

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

what molecule is required for triggering NFKB?

A

CD28 and PKC theta

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

IL-6

A

acute phase proteins, neutrophils, fever

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

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

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

IFN γ

A

macrophage killing, MHC II expression, anti-viral response

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

serum sickness

A

type III hypersensitivity

using horse Abs against foreign pathogen

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

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

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

homeostatic proliferation

A

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

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

CTLA-4

A

co-inhibitory molecule (binds B7 on APC)

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

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

naturally occurring blood antibodies are of what class

A

IgM

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

type III allergic reaction

A

IgG

activates complement/phagocytes

in serum sickness, arthus reaction

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

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

IL-2

A

drives clonal expansion and differentiation of naive T cells

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

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

type I allergic reaction

A

IgE

mast cell activation

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

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

IL-10

A

down regulates immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
proteins of CTL
* 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
26
HEV
T cells go thru it in lymph node before they meet up w an APC
27
thymocyte
T cell in thymus; not activated there to generate imunne response; don't recirculate
28
type IV allergic reaction
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
29
Tfh
activate B cells and Ab production in germinal centers
30
expression of TCR/CD3 on the membrane depends on what?
zeta chain
31
CD40-CD40L
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
CAR T cell technology
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
anti-CD3 Ab or lectin
can cross link TCR/CD3 mimicking an Ag so cells are tricked into releasing Ca/DAG
34
S1P
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
TH2
help in antibody production
36
H antigen
Backbone of ABO system (coded for by FUT1) bombay phenotype if don't have
37
cyclosporin pathway
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
ionophores
cyclical compounds that pick up/drop off Ca (chelate Ca) ex. PMA mimicks DAG, exerts similar effects
39
class I vs class II vs class III MHC
* 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
Th17
elicited by TGFβ and IL-6, express RORγT TF recruit neutrophils during early bacterial/fungal infections - abnormal activation leads to autoimmunity
41
classic hybridoma technology
to make MoAB immunize animal with Ag, collect Ab, transfer to HAT medium, select hybridoma for right Ag and then clone
42
MHC is so diverse because of
**polymorphisms** (many alleles in the population) and **polygeny** (several types of MHC molecules within 1 person)
43
can TCR-CD3 alone complete the signal?
No! it is incomplete and causes anergy - need B7 CD28 to make naive T cell fully activated
44
peptide processing in MHC II
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
A vs B antigen (biochemically)
ABO locus codes for glycosyl transferase A is N-acetylgalactosamine (A codes for N-acetylgalactosamine) B is galactose (B codes for galactose transferase)
46
peptide anchor residues
side chains of amino acid residues of the peptide fit into pockets of the peptide-binding cleft of the MHC
47
dual role of TGFβ
activates both Treg and TH17 which do oppostite things
48
IFNα/β
antiviral
49
genetics of MHC II
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
tissue transglutaminase (ttg)
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
peptide processing MHC I
**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
clonal deletion
only cells with TCR will die. the rest stay alive
53
steps of leukocyte extravasation/molecules involved
1. rolling: selectin/mucin 2. activation: chemokine 3. adhesin: integrin/CAM 4. diapedesis: PECAM
54
prolonged DTH response
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
digeorge syndrome
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
makeup of MHC II protein
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
western blotting
* take virus, dissociate with detergent * run on SDS PAGE * transfer to nitrocellulose paper and add antiserum * add anti-IgG
58
Th17
promote IL-17 mediated inflammatory response
59
makeup of MHC I protein
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
TH2 leads to release of what cytokines
IL-4 (B cell activation) IL-5 (eosinophils)
61
IL-12
T cell differentiation (TH1)
62
haplotype
each set of alleles encoding MHC inherited from a parent (theres a 1/4 chance that 2 siblings will have identical haplotypes)
63
Tc
kill tumor and virus infected cells, reject histoincompatible grafts
64
hygeine theory
early exposure to ubiquitous microorganisms plus good genes can lead to non-atopic (no hypersensitivity reaction)
65
what are the 5 classes of cytokine receptors are what are the ligands of each?
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
major vs minor cross match
major: donor RBCs + recipient serum minor: donor serum + recipient RBCs
67
TH1 leads to relase of what cytokines
IFNγ and IL-2 (T cell differentiation)
68
delayed type hypersensitivity (type IV hypersensitivity)
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
PECAM
binds to itself to mediate diapedesis
70
IL-4
B cell activation (Th2)
71
drug hypersensitivity and HLA alleles
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
type II allergic reaction
IgG Ag activates complement or receptor alters Ab signaling involved in some drug allergies, chronic uticaria

Block 6: Immuno (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions