Elevated plasma levels of IgA1, IgA1-rheumatoid factor (RF), and IgA1-containing immune complexes (IgA1-IC) have been detected in patients with a broad spectrum of diseases including IgA nephropathy (IgAN), acquired immune deficiency syndrome (AIDS), dermatitis herpetiformis (DH), Henoch-Schönlein purpura (HSP), systemic lupus erythematosus (SLE), alcoholic liver disease, rheumatoid arthritis (RA), and other diseases [1-10]. Although, tissue deposits are characteristically found in the glomerular mesangium in IgAN and/or in the skin of HSP and DH patients, they cannot always be demonstrated in tissues of patients with AIDS (4, 11).

It has been proposed that overproduction of polyclonal or antigen-specific IgA1 and/or its defective clearance may be involved in the pathogenesis of IgAN [1, 2, 12-14]. However, mere overproduction of IgA1 due to excessive stimulation is an unlikely cause of IgA1-IC and deposition of such complexes in tissues: extremely high plasma levels of IgA (up to 50 g IgA/1) in multiple myeloma does not result in tissue deposition and IgA-IC are seen only rarely. Particularly striking are differences in IgAN and AIDS: although obviously of different etiology, they share common features such as increased serum levels of IgA1, the presence of IgA1-RF and of IgA1-IC that apparently are composed of identical components (IgAl-IgG-C3); however