the traf6-nfκb signaling pathway in autoimmunity not just inflammation不仅自身免疫炎症traf6-nfκb信号通路.pdfVIP

Arthritis Research Therapy August 2005 Vol 7 No 4 Thomas Viewpoint The TRAF6-NFκκB signaling pathway in autoimmunity: not just inflammation Ranjeny Thomas Centre for Immunology and Cancer Research, Princess Alexandra Hospital, University of Queensland, Brisbane, Australia Corresponding author: Ranjeny Thomas, rthomas@.au Published: 23 June 2005 Arthritis Research Therapy 2005, 7:170-173 (DOI 10.1186/ar1784) This article is online at /content/7/4/170 © 2005 BioMed Central Ltd Recently, Akiyama et al. [1] described defects in thymic gene [4]. Thymic selection defects feature in the negative selection and in CD4+CD25+ regulatory T cell pathogenesis of many if not all mouse models of spontaneous production in mice deficient for tumor necrosis factor (TNF) autoimmune arthritis and lupus. In these models, including the receptor associated factor (TRAF)6. Signaling through cell non-obese diabetic (NOD) × K/B TCR transgenic strain [5], surface receptors to activate nuclear factor (NF)κB and the New Zealand Black (NZB) lupus-prone strain [6], and the mitogen-activated protein (MAP) kinases through adaptor SKG ZAP70 mutant model of spontaneous arthritis [7], a molecules, including TRAF6, is of critical importance to variety of defects in the interaction of APCs and thymocytes survival and activation of all cells in the body, from those interfere with the normal process of negative selection, thus regulating the immune response to epithelial cells, with which permitting the release of dan