Streptococcal M protein enhances TGF‐β production and increases surface IgA‐positive B cells in vitro in IgA nephropathy

glomerular mesangium. Several investigators have described the presence of a wide range of immunoBackground. High serum levels and enhanced in vitro production of IgA are observed in more than half of logical abnormalities in IgAN. These include the presence of high levels of antibodies [2], IgA-containing patients with IgA nephropathy (IgAN ); and transforming forming growth factor-b ( TGF-b) is certain immune complexes [3,4], and abnormal regulation of T cells [5–7]. The clinical features include spontaneous IgA class switching factor. On the other hand, macroscopic haematuria appears frequently with upper development of macroscopic haematuria with upper respiratory tract inflammation such as pharyngitis and respiratory infection as tonsillitis in IgAN. Methods. We compared the lymphocytic response tonsillitis, and the clinical course resembles, in general, that of acute glomerulonephritis (AGN ) caused by to in-vitro stimulation by group A streptococcal M proteins of apparent virulence factor between IgAN, group A streptococci. Transforming growth factor-b ( TGF-b) induces IgA non-proliferative glomerulonephritis (NPGN ), and normal subjects. M proteins were extracted from group isotype expression on surface IgA negative (sIgA−) B cell in certain B cell activation systems [8–13], and A streptococcal strain type 5 and type 12 determined serologically.