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PMCOL 200 > Immunosupressants > Flashcards

Immunosupressants Flashcards

1
Q

what are 3 applications of immunosuppressants?

A
  1. suppress rejection of donor organs/tissues
  2. suppress ‘Graft-vs-Host’ disease (GVHD)
  3. auto-immune diseases
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2
Q

what is the ‘Graft-vs-host’ disease?

A

donor lymphocytes (on graft) begin to attack host (opp rxn to transplant rejection: host->donor)

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3
Q

what causes the transplant rejection rxn?

A

antigens on donor organ are recognized as ‘non-self’ and host initiates immune response to attack it

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4
Q

what are 4 ex of autoimmune diseases?

A

rheumatoid arthritis, lupus, ulcerative colitis, psoriasis

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5
Q

t/f: cancer chemotherapeutic drugs and immunosuppressants are very different

A

false, there is great overlap btwn immunosuppressants and cancer chemotherapeutic drugs (stop rapidly dividing cells)

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6
Q

what are the 2 main phases of the adaptive immune response?

A

induction and effector

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7
Q

what are the 2 parts of the induction phase of the adaptive immune response?

A

antigen presentation and clonal expansion/maturation

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8
Q

what is the antigen presentation phase?

A

an antigen-presenting cell absorbs, processes, and expresses an antigen to a T-helper precursor cell which activates that clonal expansion and differentiation phase

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9
Q

what is the clonal expansion and maturation phase? (3)

A

T-helper precursor cells release IL-2 which has + feedback causing incr division and differentiation into T-helper 0 cells, Th0 cells secrete IL-4 (same + feedback as IL-2) and cause differentiation into Th1 and Th2 cells, Th1 cells become mature Th1 cells or cytotoxic t-cells and Th2 cells become B-cells (both by clonal expansion)

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10
Q

what is the effector phase? (3)

A

B-cells produce antibody-mediated response (Abs against Ags), T-cells produce cell-mediated response (Th1 cells secrete cytokines, cytotoxic t-cells kill infected cells)

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11
Q

what is the adaptive immune response aka?

A

specific immune response

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12
Q

what phase of the adaptive/specific immune response do most immunosuppressant drugs exhibit their effects?

A

induction phase

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13
Q

what 5 steps/mechanisms do immunosuppressant drugs target/utilize?

A
  1. inhibit IL-2 (+ feedback)
  2. inhibit cytokine gene expression (glucocorticoids)
  3. cytotoxicity (kill immune cells/prevent maturation/expansion)
  4. inhibit nucleic acid synthesis (rapid repl’n during clonal expansion)
  5. block t-cell surface receptors (Abs block Ag-presentation/immune response activation)
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14
Q

what does activation of Th0 cells require?

A

activation of calcineurin-NFAT (nuclear factor of activated t-cells) signalling pathway

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15
Q

what is that calcineurin-NFAT pathway?

A

t-cell receptor (interacts w/ APC) activation generates Ca signal (via PLC) that activates calcineurin (phosphatase) which dephosphorylates NFAT

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16
Q

what can dephosphorylated NFAT do? (3)

A

migrate to t-cell nucleus, act as a transcription factor and express IL-2 gene (for t-cell maturation/proliferation)

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17
Q

what are 2 ex of calcineurin inhibitors?

A

cyclosporine and tacrolimus

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18
Q

what are the targets of cyclosporine and tacrolimus resp.?

A

cyclophilin and FKBP

19
Q

what do drug-bound cyclophilin and FKBP do?

A

suppress calcineurin, decr NFAT transcription of IL-2 and suppress t-cell maturation/proliferation

20
Q

what do proliferation signal inhibitors do?

A

interfere w/ signals of IL-2 receptor activation

21
Q

what is a major pathway responsible for cell growth and proliferation? (affected by proliferation signal inhibitors)

A

mTOR

22
Q

what is an ex of a proliferation signal inhibitor?

A

rapamycin (aka sirolimus)

23
Q

what is the target and effect of rapamycin/sirolimus?

A

FKBP (same as tacrolimus)

24
Q

t/f: rapamycin/sirolimus has the same effects as tacrolimus when bound to FKBP

A

false, rapamycin-FKBP doesn’t inhibit calcineurin

25
Q

what does rapamycin-FKBP do?

A

inhibits mTOR (mammalian target of rapamycin) protein complex

26
Q

what are 4 effects of IL-2R activation?

A

genome replication, cell division, clonal expansion, further IL-2 expression (+ feedback)

27
Q

how does rapamycin/sirolimus-FKBP inhibit t-cell growth/proliferation?

A

targets and inhibits mTOR which decr IL-2 pathway

28
Q

what are cytotoxic agents?

A

“dirty drugs” (less specific) that interfere with DNA repl’n in rapidly dividing cells

29
Q

what is cyclophosphamide?

A

alkylating agent that generates intrastrand cross-linking btwn bases which interferes w/ DNA repl’n/division (rapidly dividing cells: cancer, immune)

30
Q

what is azathioprine?

A

purine analog so interferes w/ appropriate purine synthesis (competes for enzymes) and prevents cell repl’n/division (rapidly dividing cells: cancer, immune)

31
Q

what are 2 cytotoxic immunosuppressants?

A

cyclophosphamide and azathioprine

32
Q

what is the general structure of an antibody (Ab)?

A

2 heavy chains, 2 light chains

33
Q

what/where is the Fab vs Fc region on an Ab?

A

Fab: determines Ag specificity (variable); upper
Fc: determines antibodies class (conserved); lower

34
Q

how can Abs potentially target/treat troublesome cells?

A

Abs can be raised to recognize specific antigens on tumour/hyperactive immune cells (autoimmune) and stop them from dividing

35
Q

what is the Fc region of an Ab recognized by?

A

different immune cells (diff responses)

36
Q

what is the issue w/ using non-human Abs for treatment?

A

are recognized as non-self and targetted/degraded by our immune system

37
Q

What is the solution to the issue w/ using non-human Abs?

A

Use “chimeric” or “humanized” version of murine/mouse monoclonal Abs so host is less likely to recognize/destroy them

38
Q

What are humanized/chimerized Abs?

A

Human Fc region of Abs with foreign Fab region to resemble human Abs (decr rejection)

39
Q

What do therapeutic monoclonal Abs end w/?

A

“Mab” (human: -umab/-zumab, chimerized: -imab/-ximab)

40
Q

what is alemtuzumab?

A

humanized IgG1 Ab that binds to CD52 receptor on immune cells

41
Q

how does alemtuzumab trigger immune cell death?

A

IgG1 Fc domain (human) is recognized by phagocytic immune cells which lyse or phagocytose the cell

42
Q

t/f: alemtuzumab is a very specific immunosuppressant

A

false, it is not specific as it will destroy healthy and destructive T and B cells

43
Q

what is basiliximab?

A

chimeric mouse-human IgG1 Ab that binds to CD25 part of IL-2 receptor on activated lymphocytes

44
Q

how does basiliximab exhibit immunosuppressant effects? (2)

A

IL-2 antagonist (prevents clonal expansion) and triggers lysis/phagocytosis by phagocytic immune cells (recognize Fc region)

PMCOL 200 (27 decks)

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