Immunologic enhancement of rat renal allografts. II. Immunohistology of acutely rejecting and passively enhanced grafts.

Abstract

Unmodified renal transplants from (Lewis x Brown Norway) F(1) hybrids to Lewis rats show deposition of immunoglobulin (IgG) and complement in the arteries, which cause an acute necrotizing arteritis with ischemic necrosis of the grafts. Treatment with a single dose of enhancing antiserum at the time of transplantation prevents the arterial deposition of IgG and complement, and the vascular lesions. The enhancing antibody probably acts peripherally by blocking crucial antigenic sites in the graft vasculature, since cytotoxic alloantibody is detectable in the circulation of both control and enhanced recipients. Unmodified allografts also show deposition of IgG in glomeruli accompanied by glomerular necrosis. Immunofluorescent studies indicate that these glomerular lesions are mediated by complexes of antigen and alloantibody, and at least partially also by a nonhistocompatibility antibody directed against antigens in glomerular endothelial cells. Enhancing antiserum treatment reduces glomerular IgG deposition and thus greatly mitigates the glomerular lesion as well.