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Immunology > Week 14 > Flashcards

Week 14 Flashcards

1
Q

SHP-1 and SHP-2

A

non-receptor tyrosine phosphatases that dephosphorylize tyrosine and terminate signaling

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2
Q

IL-12

A

Activates NK cells. Induces differentiation of CD4+ cells into Th1 cells.

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3
Q

Two phases of AID SHM

A

Phase one is the deamination of C to a U that is not corrected by DNA repair mechanisms - this is later paved over as a T in later progeny.

Phase two is deamination of C to a U that is corrected by either UNG or MSH2/6

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4
Q

MSH2 / UNG double KO

A

Almost no A:T mutations. No CSR.

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5
Q

UNG deficiency

A

mainly transition mutations at G:C to A:T

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6
Q

MMR / MSH2 deficiency

A

Reduced mutations at A:T base repair

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7
Q

Chromatin modifications near DSBs

A

gamma-H2AX

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8
Q

Conrad Waddington

A

Epigenetic Landscape showing how genes affect cell development decision and instruct differential potential

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9
Q

histone modification responsible for rapid response of inflammatory genes

A

H3.3S31ph delineating gene bodies, H3.3S28ph delineating promoters and enhancers

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10
Q

Histone types

A

H3, H4, H2A, H2B and H1

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11
Q

What enzymes modify histones with acetylation?

A

histone acetyltransferases (HATs) and histone deacetylase (HDACs)

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12
Q

selectins

A

membrane glycoproteins with a distal lectin-like domain that binds specific carbohydrate groups. Members of this family are induced on activated endothelium and initiate endothelium–leukocyte interactions by binding to fucosylated oligosaccharide ligands on passing leukocytes

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13
Q

leukocyte integrins important for extravasation

A

LFA-1 (􏰀L:􏰁2, also known as CD11a:CD18) and CR3 (􏰀M:􏰁2, complement receptor type 3, also known as CD11b:CD18 or Mac-1)

Both bind to ICAM-1 and ICAM-2

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14
Q

Through what protein are integrins linked to the cyoskeleton?

A

talin

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15
Q

Weibel–Palade bodies

A

Pre-formed granules in endothelial cells that contain P-selectin. Released to cell surface in response to TNFa.

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16
Q

Epithelial cell response to TNFa

A

release of P-selectin from Weibel–Palade bodies, followed by mRNA transcription of E-selectin. Mostly E-selectin expressed after 2 hours.

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17
Q

P- and E-selectin ligands

A

sulfated sialyl-LewisX on neutrophils

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18
Q

What allows circulating leukocytes to interact with the endothelium?

A

Inflammation-induced vasodialation allows for decreased blood flow, allowing the luekocytes to slow down enough to interact with the endothelium.

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19
Q

What induces P-selectin release from endothelial cells?

A

leukotriene B4, C5a, histamine

Also LPS and TNFa, which also cause E-selectin transcription

20
Q

How are neutrophils able to roll along endothelium under such high shear from blood flow?

A

They use ‘slings’, which are long extensions of plasma membrane that wrap up around the rolling cell and slow it down.

21
Q

Molecular interactions of extravasation

A
  1. P/E-selectin and sialyl-LewisX
  2. LFA-1/CR3 and ICAM1/2
  3. Extravasation by the interaction of CD31(PECAM) on both endothelial cells and leukocytes - enzymes break down basement membrane
  4. migration under the influence of chemokines
22
Q

How do chemokines induce chemotaxis?

A

They bind to proteoglycans in the extracellular matrix and on endothelial surfaces, making a matrix-associated gradient to the infection.

23
Q

Acute-phase proteins

A

serum amyloid, CRP, fibrinogen, MBL, SP-a/D

24
Q

First protein that a newly-synthesized MHC-I binds to

A

calnexin

25
Q

Differences between terminal amino acids of peptides in MHCI or MHCII

A

MHCI is closed, so it has constant terminal amino acids. MHCII can have variable terminal amino acids

26
Q

Types of MHCII superantigens

A

Bacterial superantigens – staphylococcal enterotoxin B and A (SEB and SEA), toxic shock syndrome toxin-1 (TSST-1)

-Viral superantigens (vSAG): endogenous mammary tumor viruses

27
Q

Differences between bacterial and viral superantigens

A

viral antigens are transmembrane

28
Q

Class II MHC peptides that bind to groove before presented peptide

A

Starts with generaic ER chaperones, calnexin, BiP and the Invariant chain (Ii)

Ii targets MHCII to the endosome.

Ii is cleaved to CLIP - pH dependent

HLA-DM releases CLIP.

29
Q

Which CD3s associate with the lipid membrane in absence of activation?

A

CD3e, CD3z

30
Q

Lipid gradients for chemotaxis

A

PIP3 in front, generated by GPCR activation, PIP2 concentrated at tail end

31
Q

How does ligand binding induce TCR activation?

A

Phosphatase exclusion
TCR conformational change
The kinetic proofreading model
Mechanotransduction

32
Q

2) How does receptor activation induce downstream signaling?

A

Liquid-ordered signaling microclusters
Lipid second messengers
Calcium signaling

33
Q

How does interfacial architecture influence T cell activation and effector responses?

A

Microvilli and ligand search
Actin dynamics and mechanotransduction
Mechanopotentiation of effector responses

34
Q

Important molecules that bind to activated CD28

A

SLP76, PI3K, VAV3, Lck

35
Q

Which type of catabolism suits proliferating cells?

A

Aerobic glycolysis

36
Q

How do cancers keep proliferating?

A

By finding a way to block terminal differentiation - expression of transcription factors, mutation of chromatin-remodeling enzymes, and changes in cellular metabolism

37
Q

Two molecules other than CD25 highly upregulated on Tregs

A

CD5, CTLA-4

38
Q

Differences between birth- and death-limited selection in the GC

A

Positively selected cells divide more times if they receive stronger T cell signals (birth-driven selection), which can have a strong exponential effect•

Death-limited selection is strong against nonsense mutations in the DZ (BCR driven); death based on affinity is harder to demonstrate

39
Q

Histone methylation enzyme

A

histone methyltransferase (HMT) - methlates H3 and H4

40
Q

Active markers of histone methylation

A

H3K4, H3K36, and H3K79

41
Q

Repressive markers of histone modification associated with silencing and condensed chromatin

A

H3K9, H3K27, and H4K20

42
Q

Histone acetylation

A

regulated by the balance between histone acetyltransferases (HATs) and histone deacetylases (HDACs). Acetylation can reduce the positive charge of the lysine residues, which will then inhibit the binding between histone tails and negatively charged DNA, leaving the underlying DNA exposed. Therefore, histone acetylation is usually considered as an active histone mark

43
Q

nucleosome

A

basic unit of chromatin, with ∼147 base pairs of DNA wrapped around a protein octamer, containing two copies each of “core” histones H2A, H2B, H3, and H4

44
Q

Role of ERGIC in MHCI peptide loading

A

intracellular retention of unstable, empty, and suboptimally loaded dimers that are prevented from reaching the plasma membrane

45
Q

Which cytocolic nucleic acid sensor can directly recruit caspase-1?

A

NLRC4

Immunology (17 decks)

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