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06. HDM Test 2 > 6. Immunological Tolerance and Autoimmunity > Flashcards

6. Immunological Tolerance and Autoimmunity Flashcards

1
Q

What two fates awaits T Cells that are self reactive in the generative (central) lymphoid organ (thymus in this case)?

A

Apoptosis or they become Treg Cells

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2
Q

What two fates await any self reactive lymphocyte in the peripheral tissues?

A

Anergy

Apoptosis

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3
Q

What apoptotic pathway occurs in immature T Cells that respond to self antigens presented in the Thymus?

A

Mitochondrial apoptotic pathway.

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4
Q

What type of cells express FOXP3?

A

Tregs

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5
Q

What is caused by antigen stimulation without adequate costimulation?

A

Anergy

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6
Q

What is the given example of “checkpoint blockade” cancer therapy?

A

Treatment of patients with anti-CTLA4 and anti-PD1 that block the receptors that would lead to anergy when T Cells respond to the cancer cells.

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7
Q

What receptor that is essential for survival of all T Cells is expressed in large amounts in Tregs?

A

CD25 (IL-2α Receptor)

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8
Q

What type of cell is allowed to survive after displaying high affinity to self antigens in the Thymus?

A

FOXP3+ T Cells (which then become Tregs)

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9
Q

What mechanism protects Treg cells from being apoptosed in the Thymus?

A

They produce anti-apoptotic molecules

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10
Q

What do Tregs do when they are activated by their antigen in the peripheral tissues?

A

They inhibit nearby T and B Cells to ensure they don’t respond to that antigen.

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11
Q

Where are induced Tregs formed?

A

Outside the Thymus, in the peripheral tissues

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12
Q

What cell type shares a close developmental relationship with iTregs?

A

Th17 cells

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13
Q

When would TGF-β induce FOXP3 expression, and when would it not?

A

TGF-β would induce FOXP3 expression when IL-6 is not present. If IL-6 is present, TGF-β and IL-6 work together to form Tregs.

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14
Q

What is the function of retinoic acid in T Cell differentiation?

A

Inhibits production of Th17 cells, and stimulates de novo generation of FOXP3+ Tregs from Naive CD4+ CD25- T Cells

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15
Q

What are the main cytokines produced by Tregs?

A

IL-4, IL-10, TGF-β

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16
Q

What cell membrane proteins are downregulated in APCs after Tregs inactivate them?

What ILs are up/downregulated?

A

CD40

CD80/CD86 (B7-1, B7-2)

IL-12 downregulated

IL-10 upregulated

17
Q

What is the function of IDO?

A

Degrades tryptophan and inactivates dendritic cells

18
Q

What happens to a B Cell in the bone marrow if it has high avidity for self antigens?

What if it has low avidity for self antigens?

A

High avidity = apoptosis OR receptor editing

Low avidity = anergy

19
Q

What is the function of CD32?

A

It is an inhibitory receptor phosphorylated by Lyn, which attenuates BCR signaling. Prevents autoimmunity

20
Q

What happens when AIRE goes bad?

A

Decreased expression of self-antigens (tissue restricted antigens / TRAs) in the Thymus

21
Q

What kind of tolerance (central or peripheral) would a mutation in AIRE cause a deficiency in?

A

Central tolerance

22
Q

How does CTLA-4 on a Treg cell decrease the activity of other T Cells?

A

It binds to B7 on dendritic cells and outcompetes the T Cells for their costimulator.

23
Q

What happens when CTLA-4 doesn’t work?

A

Uncontrolled proliferation of T Cells

24
Q

What gene polymorphisms are associated most strongly with autoimmunity?

A

MHC genes

25
Q

Self reactive TCRs is not enough to trigger pathogenesis of T Cell autoimmunity. What other factor is also necessary?

Why is this necessary?

A

“Environmental Factors”

Such as infection, tissue injury, etc. Something to mobilize T Cells to the region.

Because the T Cells require activation by dendritic cells, and dendritic cells are only active as a response to environmental factors. If there are no environmental factors, the dendritic cells won’t produce CD80/86 and the self T Cell will become anergic.

26
Q

What is the cause of Rheumatic Fever?

A

Streptococcal infection leads to cross reactivity between anti streptococcal antibodies and cardiac myosin. :(

27
Q

What is the cause of Multiple Sclerosis?

A

T Cells react with Epstein-Barr, Influenza A, and Papilomavirus

28
Q

What are the three general methods that microbial antigens can use to induce autoimmunity?

A

Molecular mimicry

Polyclonal (bystander) activation

Release of previously sequestered ags.

29
Q

What exacerbates Systemic Lupus Erythematosus in mouse models?

(… and hopefully in humans as well, otherwise…)

A

Estrogens

30
Q

What two drugs can bind to RBCs and create a “neoantigen” that leads to hemolytic anemia?

A

Penicillins and Cephalosporins

31
Q

What kind of drugs can induce Multiple Sclerosis and Systemic Lupus Erythematosus in certain persons?

A

TNF-γ blockers.

06. HDM Test 2 (9 decks)

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