Abstract
A balance between an adequate immune response to an antigen or pathogen and tolerance is a prerequisite for normal immune homeostasis and the well-being of the host. In this complex self-regulation, multiple mechanisms have been implicated as contributing to the immune tolerance network, including apoptosis, anergy, and active suppression. Current excitement focuses on active suppression and new regulatory T cell-mediated pathways of immunosuppression that are being unraveled. Central to several of these pathways is transforming growth factor-beta (TGF-beta), a potent immunoregulatory cytokine that contributes to the function and generation of regulatory T cells.
MeSH terms
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Animals
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Antigens, CD
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Antigens, Differentiation / metabolism
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Autoimmune Diseases / immunology
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CD4-Positive T-Lymphocytes / immunology
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CD4-Positive T-Lymphocytes / metabolism
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CTLA-4 Antigen
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Glucocorticoid-Induced TNFR-Related Protein
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Humans
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Immune Tolerance*
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Interleukin-2 / metabolism
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Membrane Glycoproteins / immunology
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Mice
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Models, Immunological
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Receptors, Cell Surface / immunology
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Receptors, Interleukin-2 / metabolism
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Receptors, Nerve Growth Factor / immunology
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Receptors, Tumor Necrosis Factor / immunology
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T-Lymphocyte Subsets / immunology
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T-Lymphocyte Subsets / metabolism
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Toll-Like Receptors
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Transforming Growth Factor beta / metabolism*
Substances
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Antigens, CD
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Antigens, Differentiation
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CTLA-4 Antigen
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CTLA4 protein, human
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Ctla4 protein, mouse
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Glucocorticoid-Induced TNFR-Related Protein
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Interleukin-2
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Membrane Glycoproteins
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Receptors, Cell Surface
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Receptors, Interleukin-2
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Receptors, Nerve Growth Factor
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Receptors, Tumor Necrosis Factor
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TNFRSF18 protein, human
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Tnfrsf18 protein, mouse
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Toll-Like Receptors
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Transforming Growth Factor beta