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t-cell co-stimulatory pathways in autoimmunity在自身免疫t细胞co-stimulatory通路
Available online /supplements/10/S1/S3 Review T-cell co-stimulatory pathways in autoimmunity Jörg J Goronzy and Cornelia M Weyand Kathleen B and Mason I Lowance Center for Human Immunology and Rheumatology, Emory University, Woodruff Circle, Atlanta, Georgia 30322, USA Corresponding author: Jörg J Goronzy, jgoronz@ Published: 15 October 2008 Arthritis Research Therapy 2008, 10(Suppl 1):S3 (doi:10.1186/ar2414) This article is online at /supplements/10/S1/S3 © 2008 BioMed Central Ltd Abstract compatibility complex (MHC) molecule. However, stimulation T-cell activation and differentiation depend on the signal strength of the TCR alone does not induce a productive T-cell received by the T-cell receptor and on signals provided by co- response, but renders the T cells anergic. A second signal, stimulatory molecules. The most prominent co-stimulatory molecule generally provided by molecules expressed on the antigen- is CD28, which controls the activation of naïve and memory T cells presenting cell (APC), is required to optimize a T-cell by antigen presented on professional antigen-presenting cells. response. In this concept, the APC holds a central position Blocking of the CD28-CD80/86 pathway has been an appealing because of its ability to provide a co-stimulatory signal. strategy for inducing tolerance in autoimmune diseases where the disease-inducing autoantigens are not known. Although CD28 has Dendritic cells (DCs) are of part
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