Cellular immunoregulatory aspects of IgA nephropathy

Abstract

Polyclonal activation of IgA-producing B cells has been observed in the majority of patients with IgA nephropathy (IgAN) and some of their family members. The precise mechanism of such activation is presently unknown. However, abnormalities of T and B cell interactions have recently been observed in this disease. These abnormalities include the decrease of IgA-specific suppressor T cell activity and the increase of IgA-specific helper T cell activity. A T cell subpopulation with receptors for the Fc portion of IgA and with CD4 antigens (ie, T alpha 4 cells) has been proposed as a candidate of IgA-specific switch T cells that convert IgM-producing B cells to IgA-producing B cells. Further analysis of the immunogenetic mechanism and the clinical correlates of the cellular immunoregulatory aspects of IgAN is necessary to elucidate the pathogenesis of this disease.