Transplant rejection

Question 1

Hyperacute

Answer 1

Onset: within minutes

Pathogenesis: antibody mediated (type II) because of the presence of preformed anti-donor antibodies in the transplant recipient

Features: occludes graft vessels, causing ischemia and necrosis

Question 2

Acute

Answer 2

Onset: weeks later

Pathogenesis: cell-mediated due to CTLs reacting against foreign MHCs. Reversible with immunosuppressants

Features: vasculitis of graft vessels with dense interstitial lymphocytic infiltrate

Question 3

Chronic

Answer 3

Onset: Months to years

Pathogenesis: Class-I MHC (non-self) is perceived by CLTs as class I MHC (self) presenting non-self antigen

Features: irreversible. T cell and antibody mediated vascular damage (obliterative vascular fibrosis): fibrosis of graft tissue and blood vessels

Question 4

Graft-versus-host

Answer 4

Onset: varies

Pathogenesis: grafted immunocompetent T cells proliferate in the irradiated immunocompromised disease host and reject cells with foreign proteins, resulting in severe organ dysfunction

Features: maculopapular rash, rash, jaundice, hepatosplenomegaly and diarrhea. Usually in bone marrow and liver transplants (organs rich in lymphocytes) potentially beneficial in bone marrow transplant