Lecture 21: Transplantation Immunology I Flashcards
Autografts
Grafts exchanged from one part of an individual to another part of the same individual
Isograft
Grafts exchanged between different individuals of identical genetic make up (identical twins)
Allografts
Grafts exchanged between non identical members of same species
Xenografts
Grafts exchanged between members of different species
HLA Ags are _______ expressed
Co-dominantly
What Ags are particularly strong barriers to transplantation
HLA-A
HLA-B
(Class I HLAs)
The three most important Class II HLAs in transplantation are
HLA-DR
HLA-DP
HLA-DQ
Direct pathway of allorecognition
T cell receptors on recipient T cells directly recognize donor MHC molecules
Indirect pathway of allorecognition
Recipient T cells recognize donor MHC molecules that have been processed into peptides by recipient APCs
This pathway is important during chronic rejection (when number of donor APCs is too low to stimulate direct immune response)
Onset and cause of hyperacute rejection
Immediate onset caused by accidental ABO blood type incompatibility. Presents while still in surgery
-Could also occur when the recipient has been sensitized to donor MHC by previous transplants, blood transfusions or pregnancy
Onset and cause of acute rejection
Weeks to months
T cell mediated response directed against the foreign MHC. (Donor DCs migrate to lymph nodes and stimulate primary recipient response) Leukocytes infiltrate graft vessels
Onset and cause of chronic rejection
Months to years
T cell mediated process resulting from the foreign MHC “looking like” a self MHC carrying an antigen. Occurs due to occlusion of blood vessels and ischemia of organ. Macrophages infiltrate and smooth muscle proliferation is often seen
Onset and cause of graft vs host disease
Variable onset
Donor T cells in the graft proliferate and attack the recipients tissues. Most common in bone marrow transplants
Main pathway of allorecognition in Acute vs chronic rejection
Acute- mainly direct, but indirect can also play role
Chronic- Mainly indirect (Abs can also be involved, depositing complement into graft tissues)
Non immunologic allograft rejection
Damaged graft tissues release mediators which trigger several cascades leading to immediate tissue damage
- Clotting cascade generates fibrinopeptides, attracting neutrophils and macrophages
- Kinin cascade makes bradykinin causing vasodilation, increased vascular permeability