Lymphocyte Function in IgA Nephropathy

IgA nephropathy is now an accepted disease entity that is characterized by preponderant mesangial deposition of IgA [1, 2]. An increasing body of evidence suggests that the mesangial IgA deposits are likely to be either IgA polymers or IgA-dominant immune complexes [3, 4]. These IgA seem to circulate in the blood because of a frequent recurrence of this disease after renal allotransplantation [5, 6] and a rapid disappearance of IgA deposits in a grafted kidney from a donor with unsuspected IgA nephropathy [7]. The presence of such IgA in the circulation suggests an increased synthesis of IgA in patients with IgA nephropathy. Although the mechanism of immune regulation of IgA has not been fully elucidated, rapidly accumulating evidence indicates that the interaction of B and T cells plays a key role in the regulation of IgA, an isotype known to be highly T-cell specific [8]. The discussion on the altered lymphocyte function in this chapter is limited to primary IgA nephropathy because mesangial deposits of IgA are observed in various other diseases such as alcoholic cirrhosis [9].