| Literature DB >> 20538527 |
Tatsuyuki Inoue1, Hitoshi Sugiyama, Yoshiyuki Hiki, Keiichi Takiue, Hiroshi Morinaga, Masashi Kitagawa, Yohei Maeshima, Kunihiro Fukushima, Kazunori Nishizaki, Hirofumi Akagi, Yoshiki Narimatsu, Hisashi Narimatsu, Hirofumi Makino.
Abstract
Aberrant O-glycosylation of serum and tonsillar IgA1 is one of the main pathogeneses of IgA nephropathy (IgAN). However, the synthesis of underglycosylated IgA1 in tonsils has not yet been characterized. This study examined tonsillar B lymphocytes of IgAN (n=34) using tonsils derived from patients with chronic tonsillitis (n=24) and sleep apnea syndrome (n=14) as a control. Gene expression of beta1,3-galactosyltransferase (beta3GalT), and the core 1 beta3GalT-specific molecular chaperone, Cosmc, UDP-N-acetyl-alpha-D-galactosamine: polypeptide N-acetylgalactosaminyl-transferase 2, were significantly decreased in tonsillar CD19-positive B lymphocytes from IgAN patients compared to control tonsillar tissues as determined by real-time RT-PCR. Tonsillar B cell beta3GalT gene expression significantly correlated with estimated GFR and negatively correlated with proteinuria and histological injury score. Western blotting showed the protein expression of beta3GalT in the tonsils to significantly decrease in IgAN in comparison to the controls. These data suggest the downregulation of beta3GalT in tonsillar B lymphocytes to be closely associated with the clinical characteristics of IgAN. Copyright 2010 Elsevier Inc. All rights reserved.Entities:
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Year: 2010 PMID： 20538527 DOI： 10.1016/j.clim.2010.05.009
Source DB: PubMed Journal: Clin Immunol ISSN： 1521-6616 Impact factor: 3.969