MEDIATORS OF IMMUNE GLOMERULAR INJURY

Mediators of immune glomerular injury may be divided into primary and secondary. Primary mediators include antibody and T cells and secondar y include complement, infiltrating inflammatory cells, such as neutrop hils, monocytes/macrophages and platelets, coagulation system, residen t glomerular cells including mesangial, endothelial and epithelial cel ls, reactive oxygen metabolites, eicosanoids, proteolytic enzymes and a host of cytokines. Following initiation of immune glomerular injury with primary mediators, which in most cases is antibody, a complex set of interactions involving some or all of the secondary mediators occu rs in the glomerulus, ultimately leading to the clinical manifestation s of glomerular injury. The precise sequence and the mechanisms of the se interactions are not fully defined but are under intense study. The identity of the putative antigens and why and how an autoimmune respo nse develops are also not fully known.