Renal - Immunlogy Of Transplantation

Front 1

Success of transplantation is dependent on matching _____.

Which class is expressed on all nucleated cells?

Which class expressed on APC's?

Which HLA Ag's are particular strong barriers to transplantation?

Three most important pairs of class II HLA Ag's?

Back 1

MHC Ag's

MHC I

MHC II

Class I HLA's - HLA-A,B,C

HLA-DR, HLA-DP, HLA-DQ

Front 2

An individual can express up to ____ different HLA class I's.

Chance of a full sibling matching HLA Class I:

Do you need to put identical twins with transplants on immunosuppressives?

Matching for _____ Ags has the most impact on graft survival.

Back 2

6

1 in 4

No immunosuppressives needed

HLA-DR

Front 3

Why is the immune response much stronger for grafts than pathogenic Ag's?

Graft-derived peptide bound by self MHC:

Graft bound by graft: (SELF)

Complete compatibility at ___, ___, and ____ offers the best chance of success.

Back 3

each cell of the graft expresses a foreign MHC I.

MHC II

MHC I

A, B, DR

Front 4

2 sources of lymphocytes for HLA typing?

Increased CTL and T-help precursors in HLA class II typing = ______ chance for success.

ABO blood matching is NOT important for what 3 grafts?

Universal donor, universal recipient:

Back 4

spleen/lymph node (from cadaver)
peripheral blood smear, - RBC's, platelets

low chance for success

corneal, heart valve, bone/tendon

Donor: O
Recipient: AB

Front 5

Best known minor histocompatibility Ag?

Some non-immunologic factors affecting transplant success? (3)

Host vs graft response:
direct pathway: MHC _____
indirect response: MHC ____

Back 5

H-Y on Y chromosome

ischemia from excision, transport, implantation
mechanical trauma, reperfusion
damaged tissue

direct: MHC I - T cell on recipient don't recognize MHC I on donor cells
indirect: MHC II - T-cell recognizes MHC II from recipient APC's

Front 6

Timeframe and causes:
hyperacute rejection:

acute graft rejection:

Back 6

hyperacute: within minutes
blood group mismatch, previous transplant from same donor, complement activation

acute: days to weeks - reactive T-cells, dendritic cells react --> CTL formation

Front 7

Timeframe and causes of chronic graft rejection:

main pathogenic mechanism?

responsive to immunosuppressive therapy?

Back 7

chronic: months-years; occlusion of blood vessels --> ischemia --> macrophage infiltrate, smooth muscle proliferation

indirect pathway

not responsive

Front 8

Graft vs Host Disease:
which transplants can cause GVHD?

What happens?

Difference between acute and chronic?

Back 8

small bowel, lung, liver - naturally contain T-cells

donor's T-cells react with host's minor H Ag's

acute - epithelial cell death
chronic - fibrosis, atrophy of grafts

Front 9

Drug #1: inhibits T-cell proliferation, induces lymphocyte apoptosis, transcriptional inhibition of inflammatory genes:

Drug #2: blocks fxn of CD3 molecule

Drug #3: peptide isolated from fungus, inhibits Ca-dependent pathway of T-cell activation

Back 9

Drug #1: corticosteroids - prednisone, etc.

Drug #2: OKT 3

Drug #3: cyclosporine

Front 10

Drug #4: macrolide lactone isolated from Streptomyces, inhibits calcium dependent T-cell activation and translocation of NFAT to nucleus

Drug #5: macrolide from Streptomyces, blocks IL-2 mediated pathway, inhibits T-lymphocyte proliferation:

Back 10

Drug #4: tacrolimus

Drug #5: Rapamycin (Sirolimus)

Front 11

Drug #6: prodrug, derivative of 6-mercaptopurine, inhibits DNA synthesis, T-cell proliferation

Back 11

Drug #6: azathioprine (AZA)