Hyperacute: within minutes- Pre-existing recipient antibodies react to donor antigen (type II hypersensitivity reaction), activate complement- Widespread thrombosis of graft vessels → ischemia/necrosis- Graft must be removed

Acute: weeks to months- Cellular: CD8+ T cells and/or CD4+ T cells activated against donor MHC (type IV hypersensitivity reaction)- Humoral: similar to hyperacute, except antibodies develop after transplant- Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate. Prevent/reverse with immunosuppressants.

Chronic: months to years- CD4+ T cells respond to recipient APCs presenting donor peptides, including allogeneic MHC.- Both cellular and humoral components (type II and IV hypersensitivity reactions)- Recipient T cells react and secrete cytokines → proliferation of vascular smooth muscle, parenchymal atrophy, interstitial fibrosis. Dominated by arteriolosclerosis.- Organ-specific examples: Bronchiolitis obliterans (lung), accelerated atherosclerosis (heart), chronic graft nephropathy (kidney), vanishing bile duct syndrome (liver)

Graft-versus-host disease:- Grafted immunocompetent T cells proliferate in the immunocompromised host and reject host cells with "foreign" proteins → severe organ dysfunction. Type IV hypersensitivity reaction.- Maculopapular rash, jaundice, diarrhea, hepatosplenomegaly. Usually in bone marrow and liver transplants (rich in lymphocytes). Potentially beneficial in bone marrow transplant for leukemia (graft-versus-tumor effect).