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To better understand its pathogenesis, we investigated tonsillar CD5+ B cells (B-1 cells) with respect to IgA synthesis. Germinal centre (GC) B cells were isolated from the tonsils of IgAN patients and the number of B-1 cells in the GC determined by flow cytometry. GC B-1 and B-2 (CD5\u2212 B) cells were purified by cell sorter, the cells were incubated with agonist anti-CD40 MoAb and the ability for antibody production by B-1 and B-2 cells determined by ELISPOT assay. GC B-1 cells and B-2 cells were incubated with agonist anti-Fas MoAb, and apoptosis in GC B-1 cells and B-2 cells was analysed by flow cytometry. Although B-1 cells do not usually take part in the GC reaction, an increase in B-1 cell numbers was observed in the GC of tonsils from IgAN patients. These B-1 cells were likely IgA1 antibody-producing cells, since the prominent IgA subclass in IgAN is generally considered to be IgA1. Although Fas-dependent apoptosis is essential for the elimination of activated B cells, these B-1 cells showed a reduced susceptibility to Fas-mediated apoptosis. It is conceivable that activated B-1 cells may survive in the GC due to impaired apoptosis and thus produce abnormal antibodies. These findings suggest that the immune responses of B-1 cells in the tonsillar GC could thus have an impact on the pathogenesis of IgAN.<\/jats:p>","DOI":"10.1046\/j.1365-2249.2001.01431.x","type":"journal-article","created":{"date-parts":[[2003,3,11]],"date-time":"2003-03-11T10:25:28Z","timestamp":1047378328000},"page":"301-308","source":"Crossref","is-referenced-by-count":31,"title":["Increase in tonsillar germinal centre B-1 cell numbers in IgA nephropathy (IgAN) patients and reduced susceptibility to Fas-mediated apoptosis"],"prefix":"10.1093","volume":"123","author":[{"given":"S","family":"Kodama","sequence":"first","affiliation":[{"name":"Department of Otolaryngology, Oita Medical University, Hazama-machi, Oita, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Suzuki","sequence":"additional","affiliation":[{"name":"Department of Otolaryngology, Oita Medical University, Hazama-machi, Oita, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Arita","sequence":"additional","affiliation":[{"name":"Department of Otolaryngology, Oita Medical University, Hazama-machi, Oita, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G","family":"Mogi","sequence":"additional","affiliation":[{"name":"Department of Otolaryngology, Oita Medical University, Hazama-machi, Oita, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2001,12,20]]},"reference":[{"key":"2022011221100464300_b1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1159\/000183538","article-title":"Idiopathic IgA mesangial nephropathy","volume":"41","author":"D'Amico","year":"1985","journal-title":"Nephron"},{"key":"2022011221100464300_b2","first-page":"168","article-title":"IgA nephropathy: pathogenesis of the most common form of glomerulonephritis","volume":"60","author":"Emancipator","year":"1989","journal-title":"Lab Invest"},{"key":"2022011221100464300_b3","doi-asserted-by":"crossref","first-page":"377","DOI":"10.1038\/ki.1995.50","article-title":"IgA nephropathy","volume":"47","author":"Galla","year":"1995","journal-title":"Kidney Int"},{"key":"2022011221100464300_b4","doi-asserted-by":"crossref","first-page":"S149","DOI":"10.1681\/ASN.V210s149","article-title":"Macromolecular properties that promote mesangial binding and mesangiopathic nephritis","volume":"2","author":"Emancipator","year":"1992","journal-title":"J Am Soc Nephrol"},{"key":"2022011221100464300_b5","first-page":"203","article-title":"Human IgA nephritis: immunocytochemical evidence of a chronic inflammatory proliferative disorder","volume":"10","author":"Yoshioka","year":"1995","journal-title":"Histol Histopathol"},{"key":"2022011221100464300_b6","doi-asserted-by":"crossref","first-page":"1342","DOI":"10.1172\/JCI110886","article-title":"Immunoglobulin A nephropathy. 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