Glomerulonephritis immune response

An intact Th-l type immune response is required for the development of experimental anti-GBMA disease (32). IL-12 is required for the Th 1 response and mice lacking lL-12 do not develop raial disease in a model of antibody-induced glomerulonephritis (33). In contrast, mice that are genetically deficient of IFN-y —I— have increased renal damage in this model suggesting a protective effect for IFN-y. 

Over the past decade there has, as result of experimental studies, been a growing appreciation that mercury may exert an effect on the immune system. As summarized by Silbergeld and Devine [72], mercury has at least two types of effects on the immune system. First, mercury induces autoimmunity to renal basement membrane proteins, causing mercury-induced glomerulonephritis in certain strains of mice and rats. Secondly, mercury exposure impairs cell-mediated and humoral immunity by affecting Thl and Th2 responses, which in turn impairs the body s ability to effectively... 

Lindane Experimental animals Increase of sheep red blood cells induced antibody response glomerulonephritis with deposition of immune complexes Meera et al. (1992) Khurana Chauhan (2002)... 

A. Antiglomerular basement membrane antibodies Some xenobiotics may induce an immune-type glomerulonephritis associated with the occurrence of antibodies against some constituents of the glomerular basement membrane. These antibodies may be directly responsible for the nephropathy or they may be produced as a consequence of non- specific alterations of the normal glomerular basement membrane lattice. 

Due to their inhibitory effects on DNA methylation, procainamide and hydralazine can induce autoreactive T cells by upregulating the expression of lymphocyte function-associated antigen-1 (LFA-1), which causes the cells to proliferate in response to normally subthreshold stimuli, including self (Yung et al. 1995). As a result, the adoptive transfer of T cells modified by in vitro treatment with procainamide or hydralazine induces an autoimmune disorder characterized by antinuclear antibodies (ANAs) and immune complex glomerulonephritis in naive mice (Quddus et al. 1993). 

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