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Host T cells are activated in the draining lymph nodes to graft antigens by two mechanisms. Grafts contain passenger leukocytes, APC bearing both MHC and co-stimulatory molecules. Passenger leukocytes travel to the draining lymph nodes and activate recipient T cells (direct alloreactivity). Direct activation of recipient T cells is responsible for acute graft rejection that occurs in the first weeks following transplantation; effectors are primarily CTL. Symptoms of acute rejection include fever, a skin rash, impaired organ function (such as decreased urine output from a transplanted kidney), and a mononuclear (T cell) infiltrate into the graft visible on biopsy.

Indirect alloreactivity comes from uptake of graft antigens by recipient APC and presentation on self MHC. Peptides from both MHC and minor H antigens are presented by recipient APC. Effectors are usually Th1 cells that activate macrophages to cause tissue injury and scarring that can cause chronic rejection or organ failure.



HLA matching: KEINE 100%ige Prävention mölglich (Präzisität,  Minor H)
HLA-A, -B, -C
HLA-D, DQ