期刊
ARTHRITIS RESEARCH & THERAPY
卷 10, 期 -, 页码 -出版社
BMC
DOI: 10.1186/ar2414
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资金
- National Institutes of Health [R01 AR41974, R01 AR42527, RO1 AG15043, RO1 AI44142, RO1 EY11916]
- NATIONAL EYE INSTITUTE [R01EY011916] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI044142, R01AI108906] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR041974, R01AR042527] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG015043] Funding Source: NIH RePORTER
T-cell activation and differentiation depend on the signal strength received by the T-cell receptor and on signals provided by costimulatory molecules. The most prominent co-stimulatory molecule is CD28, which controls the activation of naive and memory T cells by antigen presented on professional antigen-presenting cells. Blocking of the CD28-CD80/86 pathway has been an appealing strategy for inducing tolerance in autoimmune diseases where the disease-inducing autoantigens are not known. Although CD28 has maintained its unique position, the past decade has witnessed the recognition that a large number of regulatory molecules on T cells must be stimulated to generate a fully protective immune response. These regulatory receptors differ in their preferential expression on T-cell subsets, in the ligands that they recognize, and in the signaling pathways that they trigger. They have in common the fact that they provide information on the cellular environment in which the T-cell response occurs. By intercepting these signals, we may be able to influence disease-relevant T-cell responses in autoimmune diseases while potentially minimizing broad immunosuppression.
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