different pathological roles of toll-like receptor 9 on mucosal b cells and dendritic cells in murine iga nephropathy不同病理toll样受体的角色9粘膜b细胞和树突细胞在小鼠iga肾病.pdfVIP

Hindawi Publishing Corporation Clinical and Developmental Immunology Volume 2011, Article ID 819646, 10 pages doi:10.1155/2011/819646 Research Article Different Pathological Roles of Toll-Like Receptor 9 on Mucosal B Cells and Dendritic Cells in Murine IgA Nephropathy Tadahiro Kajiyama, Yusuke Suzuki, Masao Kihara, Hitoshi Suzuki, Satoshi Horikoshi, and Yasuhiko Tomino Division of Nephrology, Department of Internal Medicine, Faculty of Medicine, Juntendo University, Tokyo 113-8421, Japan Correspondence should be addressed to Yasuhiko Tomino, yasu@juntendo.ac.jp Received 22 December 2010; Accepted 2 May 2011 Academic Editor: K. Blaser Copyright © 2011 Tadahiro Kajiyama et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Although pathogenesis of IgA nephropathy (IgAN) is still obscure, pathological contribution of mucosal immunity including production of nephritogenic IgA and IgA immune complex (IC) has been discussed. We have reported that mucosal toll-like receptor (TLR)-9 is involved in the pathogenesis of human and murine IgAN. However, cell-type expressing TLR9 in mucosa remains unclear. To address this, we nasally challenged cell-specific CpG DNA ((i): dendritic cell: (DC), (ii): B cell, (iii): both), known as ligand for TLR9, to IgAN prone mice and analyzed disease phenotype of each group. After 8 times of the weekly administration, every group showed deterioration of glomerular damage. However, CpG-A-group showed clear extension of mesangial proliferative lesions with increase of serum IgA-IgG2a IC and its glomerular depositions, while CpG-B-group showed