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Immunology Final Exam - AH > Chapter 17 - Transplants > Flashcards

Chapter 17 - Transplants Flashcards

1
Q

MATCHING:

1) autografts a) grafts exchanged b/w nonidentical members same sp.
2) isografts b) grafts exchanged b/w members of diff. species
3) allografts c) grafts exchanged from 1 part to another same body
4) xenografts d) grafts exchanged b/w identical twins

A

1 - c
2 - d
3 - a
4 - b

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2
Q

Graft rejection shows what 2 key features of adaptive immunity?

A

memory and specificity

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3
Q

what is graft rejection mediated by?

A

lymphocytes / T lymphocytes

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4
Q

what is common to all T-cells?

A

CD3

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5
Q

what HLAs are strong barriers to transplantation?

A

class I (HLA-A, HLA-B)

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6
Q

what are the 3 most important HLAs for transplantation?

A

class II (HLA-DP, HLA-DQ, HLA-DR)

remember it’s alphabetical p, q, r

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7
Q

in direct allorecognition, what does the T cell recognize?

what is it involved in?

A

UNPROCESSED allogeneic MHC from APC

primary response against graft

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8
Q

in indirect allorecognition what does the T-cell recognize?

when is this important?

A

PROCESSED peptide of allogeneic MHC molecule bound to self MHC or Professional APC

during chronic rejection when # of donor prof. APCs is low

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9
Q

what are the types of rejections in order from least time to most time taken

A

hyperacute, accelerated, acute, chronic

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10
Q

what is the cause of hyperacute rejection?

A

preformed antidonor Abs and complement

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11
Q

what is the cause of accelerated and acute rejection?

A

reactivation of sensitized T cells

primary activation of naive T cells

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12
Q

what is the cause of chronic rejection?

A

immunologic and nonimmunologic factors

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13
Q

Acute cellular rejection involves what?

A

Th1 cells

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14
Q

Acute vascular rejection involves what?

A

Th2 (humoral)

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15
Q

what kind of response does hyperacute rejection involve?

A

Humoral response

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16
Q

what is an example of hyperacute rejection?

what does it activate?

A

ABO blood group incompatibility

classical complement activation leading to death of epithelium

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17
Q

what is an example of acute rejection?

what kind of cell damage is present? by what?

A

CD4 and CD8 T cells occurs in days to weeks

parenchymal cell damage, interstitial inflammation, endothelialitis
by CTLs and DHT reactions

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18
Q

what plays an important role in triggering acute rejection?

A

Donor DCs (aka passenger leukocytes)

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19
Q

what is an example of chronic graft rejection?

what is involved and what pathway is the main pathogenic mech?

A

months to years after transplantation due to ischemia of the organ

macrophages and Abs involved, main mech is Indirect pathway

20
Q

what are some non-immunological factors in chronic rejection?

does chronic rejection respond to immunosuppressive therapy?

A

ischemia-reperfusion damage, recurrence of the disease, nephrotoxic drugs

NO

21
Q

what variables determine transplant outcome?

A

condition of the allograft (non-immunological factors)
donor-host Ag disparity
strength of host anti-donor response
immunosuppressive regimen

22
Q

when transplanted, damaged graft tissues release mediators which trigger several biochemical cascades leading to what?

A

immediate tissue damage via a clotting cascade generates fibrin and fibrinopeptides

23
Q

what do fibrinopeptides do?

A

increase local vascular permeability and serve as chemoattractant for neutrophils and macrophages

24
Q

what does the kinin cascade produce?

what do early proinflammatory responses lead to if left uncontrolled?

A

bradykinin which causes vasodilation, smooth muscle contraction, and increased vascular permeability

allograft rejection

25
Q

what is included in the donor - recipient work up?

A

ABO blood group compatibility, tissue typing (HLA), cross-matching (presence of preformed Abs), mixed lymphocyte reaction

26
Q

ABO matching is NOT important for what?

A

corneal transplantation, heart valve transplantation, bone and tendon grafts

27
Q

why is HLA compatibility between donor and recipient required?

A

due to extreme polymorphism of HLA

28
Q

the ID of HLA Ags has traditionally been done by what mechanism?

A

complement dependent serology

29
Q

what are the sources of lymphocytes for HLA typing?

A

spleen and LN from cadaver

30
Q

what doe the Ag-Ab complex activate?

A

classical complement cascade resulting in lymphocyte lysis which can be detected by staining the cells

31
Q

what is cross matching needed for?

A

to prevent hyperactive Ab-dependent rejection of graft

32
Q

how do you test for preformed Abs?

A

use a microcytotoxicity test with complement-activated cell damage
the recipient’s serum is mixed with donor cells, if no damage then could be a donor

33
Q

what is the process of the mixed lymphocyte response test?

A

leukocytes from 2 unrelated individuals are mixed, lymphocytes from the donor are irradiated to stop their proliferation and called stimulator cells

34
Q

what are stimulator cells used for?

what are responder cells?

A

presentation of class II MHC Ags

intact lymphocytes from the recipient

35
Q

how are responder cells activated?

how is the response measured?

A

by mismatched class II MHC and proliferate

tritiated thymidine

36
Q

If class II MHC Ags are the same ______?

A

no proliferation will occur (good for transplantation)

37
Q

what happens in HVG response?

A

host immune system (T cells) attacks the donor tissue (transplant)
adaptive immune response

38
Q

Is the immune response against a graft stronger or weaker than the response against a pathogen?

why?

A

much stronger because of a higher frequency of T cells that recognize graft as foreign

39
Q

What activates endothelial cells and what enters?

A

Non-immune injury of the graft (Danger Signals)

T cells enter the allograft

40
Q

what are the effector mechanisms of graft rejection?

A

Humoral rejection Th2

Cellular rejection Th1

41
Q

what happens in GVHD?

who does it happen to?

A

reaction of grafted mature T cells in the marrow inoculums with allo-Ags of the host directed against minor H Ags or recipient

immunocompromised recipients due to their inability to reject the allogenic cells in the graft

42
Q

where does GVHD occur most often?

A

small bowel, lung, liver

43
Q

What happens in acute GVHD?

what are clinical manifestations?

A

epithelial cell death in the skin, liver, and GI

rash, jaundice, diarrhea, GI hemorrhage

44
Q

What happens in chronic GVHD?

what are clinical manifestations?

A

fibrosis and atrophy of organ

organ dysfunction, obliteration of small airways

45
Q

What are the 3 immunologically privileged sites?

A

brain, testis, cornea (eye)

Immunology Final Exam - AH (6 decks)

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