Pathogenetic mechanisms in schistosomal glomerulonephritis

Glomeruli are eventually exposed to adult worm gut antigens that escape hepatic clearance and to Schistosoma-specific antibodies generated by immunocompetent cells in the liver, systemic lymphoid tissues, and spleen. This process is activated by concomitant salmonellosis via toll-like receptor 4 (TLR4) and by hepatitis C virus infection via TLR2. The predominant immunoglobulin is IgM in class I schistosomal glomerular disease, IgG in class II, and IgA in classes III and IV. Note that glomerular exposure to serum amyloid A (SAA) generated by the hepatocytes under the influence of interleukin-1 (IL-1) and IL-6 may produce class V lesions. Autoimmune mechanisms may also be involved in propagating glomerular lesions.