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Pharmacotherapy: concepts of pathogenesis and emerging treatments Co-stimulation and T cells as therapeutic targets Gizinski AM; Fox DA; Sarkar SBest Pract Res Clin Rheumatol 2010[Aug]; 24 (4): 463-77Full activation and differentiation of resting T cells into effector T cells requires at least two signals, the first through engagement of the T cell antigen receptor (TCR) by the antigen-major histocompatibility complex (MHC) on antigen-presenting cells (APCs), and the second by engagement of co-stimulatory molecules such as CD28, on T cells by ligands such as CD80/86 on APCs. Effector T cell differentiation is associated with proliferation, secretion of cytokines and expression of additional surface molecules. These inducible structures may have stimulatory (ICOS, OX40 and 4-1BB) or inhibitory (cytotoxic T-lymphocyte antigen (CTLA)-4) potential. To the extent that T cells have a role in particular immune-mediated diseases, interruption of T cell co-stimulation is a potentially worthwhile approach to the treatment of those conditions. This article summarises the experience in treating rheumatological disease by perturbation of T cell co-stimulation, and also describes structures that could be future targets for this type of therapeutic approach.|Abatacept[MESH]|Antigen Presentation/*immunology[MESH]|Antigen-Presenting Cells/immunology[MESH]|Antirheumatic Agents/immunology/therapeutic use[MESH]|Arthritis, Rheumatoid/*immunology/therapy[MESH]|B7-1 Antigen/immunology[MESH]|CD28 Antigens/immunology[MESH]|Cell Differentiation/immunology[MESH]|Clinical Trials as Topic[MESH]|Humans[MESH]|Immunoconjugates/*immunology/therapeutic use[MESH]|Immunosuppressive Agents/immunology/therapeutic use[MESH]|Lymphocyte Activation[MESH]|Receptors, Antigen, T-Cell/*physiology[MESH]|Signal Transduction/immunology[MESH]|T-Lymphocytes/drug effects/*immunology[MESH] |
