tailieunhanh - Báo cáo y học: "Direct Toll-like receptor 2 mediated co-stimulation of T cells in the mouse system as a basis for chronic inflammatory joint disease"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Direct Toll-like receptor 2 mediated co-stimulation of T cells in the mouse system as a basis for chronic inflammatory joint disease. | Available online http content 6 5 R433 Research article Direct Toll-like receptor 2 mediated co-stimulation of T cells in the mouse system as a basis for chronic inflammatory joint disease Vera Sobek1 Nico Birkner2 Ingrid Falk1 Andreas Wurch1 Carsten J Kirschning3 Hermann Wagner3 Reinhard Wallich4 Marinus C Lamers2 and Markus M Simon1 Department of Cellular Immunology Max-Planck-Institut fur Immunbiologie Freiburg Germany 2Department of Developmental Immunology Max-Planck-Institut fur Immunbiologie Freiburg Germany 3Technische Universitat Munchen Klinikum rechts der Isar Munchen Germany 4Universitatsklinikum Heidelberg Institut fur Immunologie Heidelberg Germany Corresponding author Markus M Simon simon@ Received 5 Mar 2004 Revisions requested 5 Apr 2004 Revisions received 18 May 2004 Accepted 18 Jun 2004 Published 19 Jul 2004 Arthritis Res Ther 2004 6 R433-R446 DOI ar1212 2004 Sobek et al. licensee BioMed Central Ltd. This is an Open Access article verbatim copying and redistribution of this article are permitted in all media for any purpose provided this notice is preserved along with the article s original URL. Open Access Abstract The pathogenesis of chronic inflammatory joint diseases such as adult and juvenile rheumatoid arthritis and Lyme arthritis is still poorly understood. Central to the various hypotheses in this respect is the notable involvement of T and B cells. Here we develop the premise that the nominal antigen-independent polyclonal activation of preactivated T cells via Toll-like receptor TLR -2 has a pivotal role in the initiation and perpetuation of pathogen-induced chronic inflammatory joint disease. We support this with the following evidence. Both naive and effector T cells express TLR-2. A prototypic lipoprotein Lip-OspA from the etiological agent of Lyme disease namely Borrelia burgdorferi but not its delipidated form or lipopolysaccharide was able to provide direct antigen-nonspecific .