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Immunology > Week 5 > Flashcards

Week 5 Flashcards

1
Q

TF of Plasmacells

A

IRF4, Blimp-1

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2
Q

TF of Bmems

A

Bach2

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3
Q

What chemokine receptor do B cells use to cycle between LZ and DZ?

A

CXCR4

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4
Q

Contents of Light Zone of GC

A

FDCs (appearing light because so much projections from fDC), LZ B cells, Tfh cells

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5
Q

Contents of DZ

A

Rapidly proliferating B cells

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6
Q

Cell surface markers used to differentiate between LZ and DZ B cells

A

CD83 and CD86 - high on light zone, low on dark zone

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7
Q

What is the mechanosensor that is responsible for MaDCAM-1 polarization on HEV cells?

A

Piezo1

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8
Q

How long do tissue-derived macrophages last?

A

self-renew permanently, tend to not be proliferative. Will renew from local precursors.

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9
Q

What are the four ways that macrophages phagocytose?

A

complement, antibody, antibody-complement, and apoptotic cells

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10
Q

what processes are efferocytosis critical for?

A

development, regeneration, apoptotic cell clearance

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11
Q

What are human NK markers?

A

CD3- CD56+

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12
Q

What are mouse NK markers?

A

CD3-NK1.1+

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13
Q

Is thymus required for NK cel development?

A

No

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14
Q

From which common progenitor do NK cells develop?

A

NK cell/T cell progenitor

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15
Q

What are the lymphocyte percentages of NK cells in the peripheral blood, spleen and liver?

A

5-20% in peripheral blood
~5% in spleen, abundant in liver

Over 70% in decidual tissue!

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16
Q

What are main roles of NK cells?

A

Cell-mediated killing (ADCC)

early IFNg production

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17
Q

How do NK cells kill?

A

predominantly perforin and granzymes, but can also use TNFa, Fas ligand and TRAIL

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18
Q

Which cytokine is required for NK cell development and survival throughout lifespan?

A

IL-15

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19
Q

Which cytokine augments NK cell cytolytic activity and survival during activation?

A

Interferon a/B (Type 1)

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20
Q

Which cytokines induce IFNg production in NK cells and are required for their proliferation?

A

IL-12 and IL-18

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21
Q

Which cytokine induces proliferation, increases cytotoxicity, and is used to grow NK cells in vitro?

A

IL-2

22
Q

What types of infections are NK-deficient individuals susceptible to?

A

viral infections, particularly herpesvirus.

May also be more susceptible to cancers.

23
Q

What is the “missing self” hypothesis?

A

NK cells will target cells (tumor cells or infected cells) that are not displaying MHC class I

24
Q

Why is there such variety in NK cell ‘phenotypes’ in any individual?

A

NK cells express a variety of activating and inhibitory receptors, which can pair with various adaptors (CD3, ITAMs, etc.) Very promiscuous pairing.

25
Q

What transcription factors are important for development of NK cells?

A

Id2, Nfil3 (E4BP4)

26
Q

What is the process of ‘licensing’ for NK cells?

A

Through MHC I. They must learn to be inhibited when they see MHC I. Then they can go into the periphery. Similar to positive and negative selection in T cell development. Some become anergic, and these may help to fight viruses and tumors.

27
Q

What are the two activating factors for NK cells of a virus-infected cell?

A

Sensing of a viral component on the cell membrane by an NK cell activating receptor.

NK2GD / NK2GD ligand (kill-me flags) interaction - ‘stress signals’ in target cell

28
Q

What is an example of an NK cell directly recognizing a virus particle on an infected cell?

A

Ly49H+ NK cells can recognize MCMV-derived m157 through the Ly49H protein (signaling through DAP12)

29
Q

What are the activating and inhibitory intracellular signalers in NK cells?

A

(mouse) Ly49A, C, G, I … have ITIM motfis (recruit phosphatases, inhibit responses) - almost always ligate MHC I
(mouse) Ly49D, H, L, P … have ITAM motifs (through adaptors like DAP12; recruit Sky and ZAP-70; Activate.

In humans, KIR genes have replaced Ly49 genes; also have activating and inhibitory flavors. inhibitory mostly recognize MHC I

30
Q

What is NKG2D?

A

NK sensor for cellular “stress”

C-type lectin-like
homodimer expressed on all NK cells and some CD8 T cells
Signals through DAP10

conserved between mouse and human

31
Q

What are NK2GD ligands?

A 
Markers of cellular stress
Look like MHC class I, but do not require B2m nor need a peptide for stability

induced in infected or tumorous cells. low levels on healthy cells.

32
Q

What is NK2GD ligand shedding?

A

Thought to be shed by tumor cells, but might be shed by myeloid cells surrounding tumors. Also known as MICA and MICB in humans.

33
Q

What are some cancer therapies using NK cells?

A

Prevention of NKG2D shedding by antibody that can also activate NK cells through Fc portion

Antibodies that block inhibitory markers on tumor cells.

34
Q

What is EAE?

A

Experimental Autoimmune (Myelo)encephalitis

35
Q

Why was studying EAE important for the discovery of Th17?

A

It was found that IL-23 receptor removal was important in protecting against EAE, i.e. IL-23 leads to disease. This led to the discovery of Th17.

36
Q

What was one of the first evidence of ILC?

A

Cellular sources of IL-22 in Rag-/- mice that protected against Citrobacter rodentium.

Sonnenberg found that these cells were CD3- (not T cells), NK1.1-, (not NK cells),
CD127+ (IL7R), c-kit+, CD90+ RORgt+

37
Q

What markers are ILC negative for?

A

CD3, CD5, CD19, B220, Ly6G, SiglecF, CD11b, CD11c

38
Q

Why were ILCs originally confused with NK cells?

A

Some ILCs have NK cell receptors, however, they are independent from IL-15

39
Q

What do Rag2-/-il2rb-/- mice lack

A

All T and B cells, plus no NK cells

40
Q

What do Rag2-/-il2rg (common chain)-/- mice lack?

A

All T and B, plus no NK cells and no ILCs

41
Q

What does the IL-2 common gamma chain recognize?

A

IL-2, IL-4, IL-7, IL-9, IL-15

42
Q

What do Rorc-/- mice lack

A

No RORgt cells

43
Q

Do all RORgt-dependent ILC3s express T-bet?

A

No. There are some that also express T-bet alongside RORgt.

44
Q

What are the two (or three) distinct populations of iLC3s in the intestine?

A

Both share CD90 and CD127.

T-bet+ (NKp46) has lower CCR6 has more IL-12R. May be more inflammatory. These cells seem to arise later in development

T-bet- has higher CCR6

There also may be an inflammatory ILC3 that is circulatory, that is positive for both T-bet, CCR6, and negative for CD4 and NKp46. Shown to enter CNS during inflammation

45
Q

What are the differences between the two distinct ILC3 populations?

A

T-Bet+CCR6- ILC3s seem to arise later in development (after weaning) and do not appear in germ-free mice.

CCR6+ ILC3s seem to be present before weaning and without microbial stimuli (LTi cells)

46
Q

What are CCR6+ ILC3s?

A

LTi cells and LTi-like cells. Require RORgt. Heterogenous in CD4 expression. Initiate lymph organ development with LTo through LTaB.

47
Q

How does fate mapping work?

A

You can cre/flox a reporter gene that will be permanently removed if the cre-ed gene is ever expressed.

48
Q

How to ID ILC1 in the gut?

A

T-bet+NK1.1+NKp46+ cells that are negative for Eomesodermin and fate map negative for RORgt

49
Q

What are the shared cell markers of ILCs?

A

CD25 (IL2Ra), CD127 (IL-7R), CD90 (Thy.1)

NK cells are an exception.

50
Q

What do ILCs require for development?

A

Development independent of Rag1/2 or thymus, but require the IL-7R and the common-gamma chain

Also require Id2 for development and progenitors in the BM (and liver for LTi cells)

51
Q

What is an example of the adaptive immune system controling ILCs?

A

At weaning, there is a massive STAT3 activation in the epithelial cells of mice that is thought to be downstream of IL-22 signaling. This is resolved by 9 weeks. However, this resolution is not apparent at 9 weeks in Rag-/- mice, indicating that they have continued IL-22 signaling without an adaptive immune arm.

52
Q

What are some ways that the adaptive immune system can affect ILCs?

A

Competition for pro-survival cytokines
control of the microbiota
Tregs might lower IL-23
IL-10 production.

Immunology (17 decks)

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