Abstract
T cells exert a fundamental role in different autoimmune chronic inflammatory diseases. The low-affinity autoreactive T cell clones provide the first amplification loop after the antigen (AgX) presentation, and if not counterregulated by the T regulatory cells (Treg), they maintain the inflammation and predispose to organ damage. Interrupting the T cell amplification loop through calcineurin antagonists leads to maintenance of the whole process under the autoimmune threshold.
MeSH terms
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Arthritis, Rheumatoid / drug therapy
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Arthritis, Rheumatoid / immunology
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Autoimmune Diseases / drug therapy*
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Autoimmune Diseases / immunology
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CD28 Antigens / physiology
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Colitis, Ulcerative / drug therapy
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Colitis, Ulcerative / immunology
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Cyclosporine / pharmacology*
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Cyclosporine / therapeutic use
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Cytokines / physiology
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Dermatomyositis / drug therapy
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Dermatomyositis / immunology
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Humans
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Immune Tolerance
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Immunosuppressive Agents / pharmacology*
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Inflammation / immunology
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Lupus Erythematosus, Systemic / drug therapy
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Lupus Erythematosus, Systemic / immunology
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T-Lymphocytes / drug effects*
Substances
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CD28 Antigens
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Cytokines
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Immunosuppressive Agents
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Cyclosporine