Abstract
B cells have been shown in various animal models to induce immunological tolerance leading to reduced immune responses and protection from autoimmunity. We show that interaction of B cells with naive T cells results in T cell triggering accompanied by the expression of negative costimulatory molecules such as PD-1, CTLA-4, B and T lymphocyte attenuator, and CD5. Following interaction with B cells, T cells were not induced to proliferate, in a process that was dependent on their expression of PD-1 and CTLA-4, but not CD5. In contrast, the T cells became sensitive to Ag-induced cell death. Our results demonstrate that B cells participate in the homeostasis of the immune system by ablation of conventional self-reactive T cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigens, CD / biosynthesis
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Antigens, CD / genetics
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Antigens, CD / immunology
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Antigens, Differentiation / biosynthesis
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Antigens, Differentiation / genetics
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Antigens, Differentiation / immunology
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Autoantigens / biosynthesis
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Autoantigens / immunology*
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Autoimmunity / physiology*
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B-Lymphocytes / immunology*
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B-Lymphocytes / metabolism
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CD5 Antigens / biosynthesis
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CD5 Antigens / genetics
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CD5 Antigens / immunology
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CTLA-4 Antigen
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Cell Proliferation
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Clonal Deletion / physiology*
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Gene Expression Regulation / immunology*
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Homeostasis / immunology
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Mice
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Mice, Transgenic
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Programmed Cell Death 1 Receptor
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T-Lymphocytes / immunology*
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T-Lymphocytes / metabolism
Substances
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Antigens, CD
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Antigens, Differentiation
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Autoantigens
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CD5 Antigens
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CTLA-4 Antigen
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Cd5 protein, mouse
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Ctla4 protein, mouse
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Pdcd1 protein, mouse
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Programmed Cell Death 1 Receptor