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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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