Transplantation Pathology Flashcards
What is the major barrier to transplantation
Rejection of the graft bc of the recipients immune system recognizes the graft as being foreign and attacks it
Which structures play a role in rejection
Cell mediated bodies
Circulating bodies
Features of the T cell mediated rejection
Involves destruction of graft cells by CD8+ CTLs
Delayed hypersensitivity reactions triggered by activated CD4+Helper cells
2 pathways : direct or indirect
What happens in direct pathway of cellular rejection
Recognizes donor MHC on surface of APCs in the graft
CD8+ recognize MHC 1 — active T cell — kill graft cells
CD4 recognize MHC 2 — proliferate , cytokines trigger delayed HS
What happens in the indirect pathway of cellular rejection
Recognition after Ags are presented by own APCs
Result is delayed hypersensitivity
2 forms of Ab mediated reactions (humoral)
1- Hyperacute rejection occurs when preformed anti donor ab are present in the circulation of the recipient
2- exposure to the class 1 and 2 HLA ag of the donor graft may evoke ab— may cause complement dependent cytotoxicity, inflammation and ab cell mediated cytotoxicity
In the 2nd form of humoral rejection initial target of ab in rejection is which structure
Graft vasculature
What is the most common organ that transplanted
Kidney
Rejection reactions of kidney classified how?
Hyperacute
Acute
Chronic
What happens in Hyperacute reaction
Ig and complement are deposited in the vessel wall causing endothelial injury and fibrin platelet thrombi
Fibrinoid necrosis
In OR room
What happens in Acute rejection
Cellular or humoral mechanism may predominate
Associated with vasculitis, Ag-Ab complexes play a role
1- Cellular= mononuclear infiltration, CD8 and CD4 cells , acute tubular necrosis,endotelitis
2- Humoral= mediated by anti donor ab, C4d is a strong indicator of humoral rejection
What happens in Chronic rejection
Vascular changes , Interstitial fibrosis ,Tubular atrophy ,Glomeruli may show scarring , duplication of basal membranes
Intimate fibrosis with vascular thickening leading to ischemic changes.
Both T-cell and humoral mechanisms involved
Two modes of Liver transplants
Acute= mixed inflammatory portal and central vein infiltrates
Chronic= continued inflammation, portal fibrosis,arteriolar thickening and bile ductular necrosis occurs
Two modes of Heart transplants
Acute cellular= lymphocytic infiltrates and possible myocardial fiber necrosis
Acute vascular= Ig deposition occurs in small arteries and produces a vasculitis
**What happens in Bone marrow transplants
HLA matching**
A distinct problem is graft versus host disease (GVHD) results from the donor lymphocytes attacking the recipient tissues having the offending HLA ag
