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lüll Prospects for antigen-specific tolerance based therapies for the treatment of multiple sclerosis Turley DM; Miller SDResults Probl Cell Differ 2010[]; 51 (ä): 217-35A primary focus in autoimmunity is the breakdown of central and peripheral tolerance resulting in the survival and eventual activation of autoreactive T cells. As CD4(+) T cells are key contributors to the underlying pathogenic mechanisms responsible for onset and progression of most autoimmune diseases, they are a logical target for therapeutic strategies. One method for restoring self-tolerance is to exploit the endogenous regulatory mechanisms that govern CD4(+) T cell activation. In this review, we discuss tolerance strategies with the common goal of inducing antigen (Ag)-specific tolerance. Emphasis is given to the use of peptide-specific tolerance strategies, focusing on ethylene carbodiimide (ECDI)-peptide-coupled cells (Ag-SP) and nonmitogenic anti-CD3, which specifically target the T cell receptor (TCR) in the absence of costimulatory signals. These approaches induce a TCR signal of insufficient strength to cause CD4(+) T cell activation and instead lead to functional T cell anergy/deletion and activation of Ag-specific induced regulatory T cells (iTregs) while avoiding generalized long-term immunosuppression.|Animals[MESH]|Antibodies, Monoclonal/therapeutic use[MESH]|Autoantigens[MESH]|Autoimmunity[MESH]|CD4-Positive T-Lymphocytes/immunology[MESH]|Carbodiimides[MESH]|Encephalomyelitis, Autoimmune, Experimental/immunology/therapy[MESH]|Humans[MESH]|Immunity, Mucosal[MESH]|Immunosuppression Therapy/*methods/trends[MESH]|Mice[MESH]|Multiple Sclerosis/*immunology/*therapy[MESH]|Peptides/immunology[MESH]|Receptors, Antigen, T-Cell/immunology[MESH]|Self Tolerance[MESH]|T-Lymphocytes, Regulatory/immunology[MESH] |