The acute and chronic rejection of transplanted organs is a serious limitation to this life-saving surgery. Rejection generally follows a typical immune inflammatory response of the patient against the transplanted organ. In the case of bone marrow transplantation, the transplanted tissue can also mount an immune response against the recipient (graft versus host disease). The interferons play an important role in each of these rejection events. The role of interferon-α in the rejection of heart¹ , bone marrow², and kidney³ transplants was indicated by the significantly poorer prognosis for transplanted patients undergoing interferon-α therapy for viral infections or cancer.

The role of interferon-γ in heart transplantation rejection was suggested by interferon-γ receptor studies ⁴ and by association of bone marrow rejection with interferon-γ gene mutations⁵. In animal studies, kidney graft survival was significantly enhanced by treatment with anti-interferon-γ antibodies ⁶ and in clinical studies, corneal transplants were successfully protected with anti-interferon-γ antibody containing eye drops ⁷.