Ideas on the immunopathogenesis of glomerulonephritis are evolving to embrace a concept of a dynamic and constantly fluctuating involvement of immune reactants in the production of glomerular inflammation. The glomerulus should be regarded as a template around which the antibody-induced inflammatory events that constitute glomerulonephritis are initiated. Such lesions may be produced by direct antibody attack on glomerular antigens of either intrinsic structural or "planted" type, as discussed in this review, or by the deposition of circulating soluble immune complexes containing extraglomerular antigens. These mechanisms are not mutually exclusive and both may play a role in some situations. Intrinsic glomerular antigens are being increasingly better defined as to site, structure, function, and experimental animal models of spontaneous and induced glomerular injury resulting from direct antibody binding to nonclassic GBM capillary wall antigens are available for study. Similar nonclassic GBM antigens are likely to be found of importance in man. Anti-GBM antibody-induced glomerulonephritis continues to be the best understood example of direct attack on the glomerulus by antibody, and its nephritogenic noncollagenous GBM antigenic constituents are being characterized. The incorporation of extraneous substances as "planted" antigens within glomerular structures is now recognized in experimental animal models, and there is suggestive evidence to support the concept in man. Emphasis needs to be placed on the continuing interplay of free antibody and antigen with deposited reactants which, together with complement components, modulate the quality and quantity of the glomerular immune deposits.