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Host Defense > Test 1, deck 3 > Flashcards

Test 1, deck 3 Flashcards

1
Q

3 types of B cells

A

conventional B2 cell
innate-like B1 cell
innate-like marginal B cell

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2
Q

what are B1s directed against? where are they made? where are they found? what are 3 other important distinguishing characteristics

A
  • directed against carbs
  • made in fetal liver- live forever
  • found in peritoneal & pleural cavities
    1) no isotype switch
    2) no somatic hypermutation
    3) no memory
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3
Q

4 factors that influence immunogenicity

A

1) larger antigen
2) route of injection- subcutaneous
3) particulates are better
4) attached to adjuvant

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4
Q

what is an adjuvant?

A

a substance that enhances the body’s immune response to an antigen- e.g. Alum

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5
Q

important components of B-cell activation when they’re T-cell dependent

A
  • need 2 signals after antigen binds BCR, and is presented in MHC class II
    1) interaction of TCR with MHC/peptide complex
    2) costimulatory molecules 40/40L
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6
Q

what happens with the activation of T cells in the presence of antigen-bound B cells?

A

T cells secrete cytokines (4, 5, 6) drive b-cells into proliferation, then differentiation as memory cells & plasma cells

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7
Q

where do B cells proliferate?

A

in germinal centers (sites within 2* lymphoid organs- lymph nodes & spleen)

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8
Q

T/F B and T cells recognize the same antigen

A

TRUE- but not the same epitope

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9
Q

primary vs secondary activation

A

primary- slow- IgM

secondary- fast- IgG

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10
Q

how does affinity increase?

A

increases as a result of somatic hypermutation at the end of primary response

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11
Q

what is the enzyme required for isotype switch?

A

AID (activation-induced cytidine deaminase)

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12
Q

when and where does isotype switch occur?

A

occurs in T-cell dependent responses, is regulated by T-cell cytokines; is in germinal center in 2ndary lymphoid tissues

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13
Q

where do VDJ rearrangements occur?

A

bone marrow & thymus (primary lymphoid tissues)

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14
Q

what 3 things happen in germinal centers?

A
    • B cell proliferation & differentiation **
  • somatic hypermutation
  • class switch
  • determination of memory vs. plasma
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15
Q

where in the germinal center does hypermutation occur?

A

dark zone

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16
Q

where in the germinal center are bad hypermutations recognized?

A

light zone

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17
Q

after hypermutation, cells with high affinity for foreign antigens are rescued from cell death by

A

follicular dendritic cells with bound antigen

18
Q

T/F You see a higher rate of antibodies with somatic mutations in T-independent antigens

A

FALSE- consequently, lower affinity

19
Q

what does the t-independent activation of b cells normally respond to

A

bacterial polysaccharide antigens which can be cross-linked (little memory)

20
Q

what does the t-independent activation of b cells normally respond to

A

bacterial polysaccharide antigens which can be cross-linked (little memory)

21
Q

what is immunological tolerance?

A

non-responsiveness to specific antigens (NOT immunosupression)

22
Q

what are some examples of tolerance?

A
  • antigens from self tissues
  • food
  • commensal bacterium
  • pregnancy
23
Q

3 mechanisms of peripheral tolerance

A

1) regulatory t cells
2) myeloid derived suppressor cells (MDSCs)
3) clonal anergy

24
Q

how are non-thymic self-antigen reactive cells eliminated?

A

AIRE induces expression of wide range of genes expressed in other organs- e.g. endocrine gland

25
Q

what is an example of a failure of central tolerance?

A
  • loss of functional AIRE gene
  • APS- autoimmune polyendocrine system
  • endocrine organs destroyed by antibodies/lymphocytes
26
Q

three types of T regs, where they’re from, what they recognize

A
  • nTregs- thymus- self-antigens, F+
  • iTregs- peripheral- foreign, F+
  • Tr1’s- peripheral, lots of IL-10, F-
27
Q

what do nTregs express? what do they require?

A

CD25, IL-2R

REQUIRE IL-2 for survival

28
Q

In what disease if foxp3 mutated?

A

IPEX- multiple tissue damages caused by self-reactive T-cells; treated with bone marrow transfer

29
Q

where are nTregs converted? which epithelial signal is important for differentiation?

A

in hassall’s corpuscle; TSLP

30
Q

under what conditions do iTregs form? what happens if the conditions are not ideal?

A
  • iTregs and Th17 both require TGFbeta
  • presence of vitamin A, IL-2 induce iTreg (Foxp3)
  • presence of inflammatory cytokines (IL-6) inhibit (ROR)
31
Q

what do Th1 cells produce?

A

immunosupressive cytokine IL-10

32
Q

what induces the production of Th1?

A

Tgf-beta and IL-27, high levels of Il-10

33
Q

T/F Direct cell to cell contact is essential for ALL t-regs

A

TRUE- CTLA-4 plays a significant role

- FoxP3+ Tregs use soluble factors (TGFbeta and IL-10 to enhance function)

34
Q

what is clonal anergy?

A

T-cells that are unresponsive to antigenic stimulation; occurs when the CD28-B7 signal is missing

35
Q

what happens when antigen is presented by B7 negative APCs?

A
  • induction of silencing process

- signaling molecules are degraded

36
Q

what is CTLA-4?

A

molecule that competes with CD28 to bind B7- will win because it has a higher affinity

37
Q

when do you see CTLA-4?

A
  • in natural sequence of antigen activation of T-cells, progressively increases
  • have constitutively high expression on T-regs
38
Q

what are MDSCs?

A

myeloid-derived suppressor cells- the firefighters called to the sight of inflammation to tone it down

39
Q

how do MDSCs get activated/work?

A
  • they respond to pre-existing inflammations & cytokines such as IFN-gamma
  • they suppress immune response, even in tumors (BAD)
40
Q

what is the diversity of nTreg antigen recognition like?

A
  • mostly self-antigens b/c they’re generated in the thymus
41
Q

three types of T regs, where they’re from, what they protect

A
  • nTregs- thymus- self-antigens, F+
  • iTregs- peripheral- foreign, F+
  • Tr1’s- peripheral, lots of IL-10, F-

Host Defense (6 decks)

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