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Micro/Immuno Part 3 > Transplant Immunity > Flashcards

Transplant Immunity Flashcards

1
Q

transplant rejection

A

-when a kidney is transplanted and the recipients T cells attack the transplant

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2
Q

graft versus host disease

A

-bone marrow is transplanted and the T cells in the transplant attack the recipients tissue

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3
Q

MHC

A
  • class I and class II genes
  • antibodies against class I were easy to if
  • tasmanian devil tumors wouldn’t transfer if there was an MHC barrier-there isn’t
  • class I and class II isotypes range from monomorphic to highly polymorphic
  • hard to get HLA match
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4
Q

blood group antigens

A
  • blood is most common transplant
  • blood groups are antigens of the surface of most cells in the body
  • most people have natural antibodies against other blood groups
  • IgM antibodies
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5
Q

o antigen

A

-mostly naked

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6
Q

a antigen

A

-galnAc

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7
Q

b antigen

A

gal

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8
Q

Rh factor

A
  • if neg, only have anti Rh after exposed to Rh-like mom giving birth to Rh pos baby
  • if pos, don’t have anti Rh
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9
Q

blood types and transplantation

A
  • ABO, method agglutination
  • AB patient has no anti A or B
  • a patient has anti B
  • B patient has anti A
  • O patient has anti A and B
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10
Q

hyperacture rejection

A
  • most severe and immediate
  • caused by preformed antibodies that react to the transplanted organ
  • most common antigen would be a blood group antigen
  • under some conditions, can have pre-existing antibodies to HLA antigens
  • minutes to hours
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11
Q

example of hyperacute

A
  • healthy kidney grafted into patient with defective kidney and pre-existing antibodies against donor blood group antigens
  • antibodies against donor blood group antigens bind vascular endothelium of graft, initiating IF response that occludes blood vessels
  • graft becomes engorged and purple colored because of hemorrhage
  • usually IgM against blood group but can be IgG against HLA
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12
Q

cross match

A
  • preformed antibodies to HLA
  • IgG
  • previous surgeries/transplants and could be exposed to HLA
  • blood transfusions- exposed to B and T cells
  • women giving birth-mom becomes sensitized to babies (dads) HLA
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13
Q

panel reactive antibody

A
  • serum of a recipient is tested against a panel of leukocytes from many individuals
  • detection of the presence of antibodies to HLA
  • presented as a percentage from 0-100%
  • have to consider past medical history-25yo w/ tetrology of fallot may not be as good as 65yo with no previous surgery
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14
Q

acute rejection

A
  • process in which T cells from recipient become reactive against the transplant
  • days to weeks
  • stronger response is donor MHC II in the graft eliciting a response (DCs in kidney- kidney cells wouldn’t normally have MHCII)-direct- DCs go to spleen and activate T cells that go back to kidney and kill it–>
  • weaker response is indirect presentation of dying donor cells by APCs-indirect
  • most immune suppression therapies are directed toward inhibiting acute rejection
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15
Q

allorecognition

A

-same species, different MHC

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16
Q

chronic rejection

A
  • months or years
  • result of indirect recognition of transplant
  • MHC or minor transplantation antigens
  • presence of antibodies to HLA class I antigens in the graft and acts on the vasculature of the graft
  • alloantibodies (against graft) recruit IF cells to blood vessel walls
  • increasing damage allows immune effectors to ender the tissue of the blood wall and inflict more damage
  • blood vessel swells
17
Q

preventing rejection-matching HLA

A
  • important but not critical aspect of graft survival
  • blood matching will suffice if needed
  • better matching increases survival of transplant
  • but only 9-13 years from 0-6 matches and 17-33%–is that actually a lot?
  • hard to match with the number of polymorphisms
18
Q

testing at transplantation

A
  • ABO repeat on donor
  • HLA I and II on donor
  • find match on computer net- to call recipient
  • cross match on all positive sera from antibody screening
19
Q

workup for transplanation

A
  • HLA type I
  • should find 6 type I antigens unless there is homozygosity
  • 2 A, 2B, 2C loci
  • HLA type II (DR) (D loci)
  • panel reactive antibody
  • mixed lymphocyte reaction
  • molecular techniques
20
Q

anti ABC testing

A
  • anti HLA-ABC done monthly on recipient
  • presensitiztion by graft, transfusion, pregnancy
  • used to cross matching against donor lymphocytes
21
Q

corticosteroids

A
  • relatives of cortisol interfere with TF for T cells
  • prednisone and prednisolone
  • dec TNF, CSF, phospholipase A, adhesion molecule
22
Q

cytotoxic drugs

A
  • interfere with DNA synthesis
  • interfere with rapid proliferation needed for immune responses
  • azathioprine is purine analog
23
Q

FK 506 and cyclosporine

A
  • natural products isolated from microbial cultures
  • inhibit signaling pathways for T cells to turn on their genes for activation- IL 2 secretion
  • FK506 is tacrolimus, prograf
  • cyclosporine is neoral
  • reduces IL2, 3, 4, GMCSF, TNF a, no T cell cytokines means no B cell division, no antigen driven division, apoptosis of activated B cells
24
Q

antilymphocyte

A
  • thymocyte globulin
  • antibodies raised in rabbits and horses directed against T cells
  • no serum sickness usually because you’re killing the T cells
25
Q

monoclonal antibodies

A
  • several preps
  • anti CD3, visilzumab, muromonabCD3
  • daclizumab and basiliximab target IL 2 receptor and inhibit activated T cells
26
Q

CTLA4 IG

A
  • soluble CTLA because has constant region of IgG and extracellular portion of CTLA4
  • blocks co stim of T cells
  • less nephrotoxic than cyclosporine
27
Q

downside of rejection therapies

A
  • infections
  • bacterial
  • fugal
  • viral
  • parasitic
28
Q

bone marrow transplant

A
  • allogenic or autologous
  • autologous can be used for solid tumors because the bone marrow doesn’t have tumors-take it out, kill tumors, put it back
  • need a really good match for allogenic
  • lots of leukemias
  • prone to GVHD
29
Q

GVHD

A
  • allogenic bone marrow transplant has mature and memory T cells
  • T cells get to secondary lymphoid tissue (lymph nodes, spleen, tonsils), interact with DC and proliferate
  • effector CD4 and CD8 cells enter tissues inflamed by conditioning regimen and causes further tissue damage

(donor cells proliferate in using DCs, go back and kill our cells)

  • some GVHD seems to help in adults who have their own T cells, if for leukemia can kill residual tumor
  • irradiate for DiGeorge because they have no T cells
  • has phases

Micro/Immuno Part 3 (12 decks)

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