There is now convincing evidence to suggest that most forms of glomerulonephritis and tubulointerstitial nephropathy involve the immune system in the destructive process. Such involvement can be mediated by a humoral immune response, a cell-mediated immune response, or a coordinated response of both limbs of the immune system derived from complementary T- and B-cell interactions. The humoral or B-cell response consists of an elaboration of antibody capable of recognizing and binding to relevant epitopes or antigenic determinants. Such an immune interaction may result in antibody binding with an intrinsic component of the glomerulus or tubulointerstitium, or with exogenous, nonrenal antigen previously sequestered within the kidney, or with circulating antigen to form circulating immune complexes that are subsequently deposited within the kidney. Such immune deposit formations typically initiate a host of amplifying inflammatory responses, including complement activation and prostaglandin release. The role of the T cell in the immunopathogenesis of renal disease is complex and not fully appreciated. T cells, under most conditions in which there is a humoral response to a complex antigen, induce or provide help to the B-cell repertoire. In some circumstances, the helper T lymphocytes also induce or stimulate the direct action of effector T cells, producing cytotoxicity and delayed-type hypersensitivity. They also influence the immunoregulation of complementary B- and T-cell functions by antigen-specific or idiotype-specific suppressor T cell interactions.
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