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Host Defense > Lecture 11: Cellular basis for immunological tolerance > Flashcards

Lecture 11: Cellular basis for immunological tolerance Flashcards

1
Q

Define immunological tolerance:

A

non-responsiveness to specific antigens

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2
Q

What are some examples of tolerance?

A

antigens from self-tissues, foods, commensal bacterium, pregnancy

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3
Q

What is the relationship between tumors and immunological tolerance?

A

tumors impair anti-tumor immunity

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4
Q

What is the relationship between tumors and immunological tolerance?

A

tumors impair anti-tumor immunity

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5
Q

Tolerance is induced by what two mechanisms?

A

1) Central

2) Peripheral

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6
Q

What is central tolerance?

A

elimination of T cells that are reactive to antigens present in the thymus (self antigens)

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7
Q

What is peripheral tolerance?

A
  • Tregs (impose suppression to other T cells and accessory cells)
  • MDSCs (myeloid derived suppressor cells) myeloid cells that become potent immunoregulatory cells when exposed to inflammatory cytokines like IFNy and kill activated T cells to prevent further stimulation
  • Anergy (when T cells are stimulated in a manner that are not “complete” cells become non-responsive to further stimulation
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8
Q

What gene allows for thymic negative selection?

A

AIRE

enables stromal cells to express non-thymic genes and present self-antigens to developing thymocytes

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9
Q

What is Hassall’s corpuscles important for?

A

site for generation of regulatory T cells

(cells that have intermediate affinity to self-antigens and are not eliminated by negative selection mature into Foxp3 Tregs)

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10
Q

What happens in patients without AIRE?

A

severe auto-recessive genetic autoimmune disorder

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11
Q

What are nTregs?

A

professional T regulatory cells that impose suppression of other immune cells (T cells)

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12
Q

nTregs antigen diversity is limited to _______

A

self antigens (generated in the thymus due to high affinity against antigens present in the thymus)

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13
Q

What are iTregs?

A

Tregs that can be manipulated by environment (food), commensals, pathogens, tumor

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14
Q

iTregs are induced by APCs that are present where?

A

mucosal environment (intestine)

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15
Q

What are cofactors to induce iTregs?

A

Vitamin A and/or D

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16
Q

What inflammatory cytokine is INHIBITORY for induction of iTregs?

A

IL-6

17
Q

Which 2 cytokines play a major role in iTreg development?

A

IL-2

TGFb

18
Q

What are Tr1 cells?

A

produce immunosuppressive IL-10

and are produced by high amounts of IL-10

19
Q

Which two cytokines induce development of Tr1 cells?

A

TGFb

IL-27

20
Q

Are Tr1 cells Foxp3+?

A

NO

21
Q

What disease results from failure of peripheral tolerance?

A

IPEX (immune dysregulation, polyendocirnopathy, enteropathy, X-linked)

22
Q

What is IPEX?

A 
systemic autoimmunity (in the 1st year of life)
characterized by LOSS of Foxp3
23
Q

What are MDSCs?

A

Myeloid Derived Suppressor Cells (heterogeneous population of cells that are defined by myeloid origin and ability to potently suppress T cell responses)

24
Q

What cytokine can activate MDSCs?

A

IFNy (usually around from pre-existing inflammation)

25
Q

MDSCs are promising therapeutically for what?

A

anti-tumor responses or to inhibit immune responses for treatment of autoimmune disease or transplant rejection

26
Q

When might a cell be “partially stimulated” and undergo anergy?

A

When naive T cells are presented antigens in the absence of the CD28 second signal

27
Q

Why do cells that get antigen but not via CD28 signaling die?

A

because the ligand for CD28 (CD80, 86) is only on a few APCs so when T cells get antigen from other cells, it isn’t right.

28
Q

What is CTLA-4?

A

something expressed by T cells after activation and competes with CD28 for B7 binding

29
Q

What has a higher affinity for B7, CD28 or CTLA-4?

A

CTLA-4 (wins the competition) and recruits signaling molecules that suppress TCR signaling/blocking antigen activation

30
Q

How are CTLA-4s used to prevent runaway T cell proliferation?

A

CTLA-4 production increases during antigen-activation of T cells (so it will bind to B7 and outcompete T cell)

31
Q

How are CTLA-4s used in graft vs host disease?

A

used to block T cell activation from the outside

accomplished via CTLA-4 IG

Host Defense (21 decks)

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