The Biology of IgA Mucosal Immunity

Abstract

The body of clinical and experimental evidence relating to the pathogenesis and course of IgA nephropathy is consistent with the development of a mucosally derived IgA immune complex-mediated disease process. Of course, to obtain conclusive evidence for immune complex pathogenesis, it is necessary to demonstrate that the same antigen and antibody present in the serum are also present in glomerular mesangial deposits. Although this proof does not currently exist for antigen, the evidence strongly supports the view that the immunoglobulins deposited in the glomeruli are the same as those in circulating complexes. It is of value to note that, although a number of experimental animal models of IgA nephropathy can be attributed to the continued mucosal administration of antigen, no such direct evidence exists in man. However, the frequent observation of recurrent infections of the upper respiratory tract, often preceding renal involvement, suggests a possible etiopathologic pattern for IgA nephropathy. Such a sweeping view is not without obvious pitfalls and the occurrence of mesangial polymeric IgA deposits secondary to impaired hepatic function highlights this. Indeed, Clarkson and his colleagues regard IgA nephropathy as a syndrome rather than an immunopathologic entity [17].