Abstract
Transgenic mice that constitutively expressed murine IL-2 in islet beta cells (RIP-IL-2 mice) had pancreatitis from birth which resolved into a peri- and intra-islet infiltrate in adult animals. In spite of the impressive infiltration, these mice did not develop autoimmunity to islet antigens. Neither was autoimmunity found to extrathymic H-2Kb molecules known to induce tolerance by a peripheral mechanism, when IL-2 and H-2Kb were coexpressed in the beta cells. Apparently, IL-2 can only act on activated T cells and is unable to reverse tolerance in T cells that have been made unresponsive through inappropriate antigen presentation in our system.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antigen-Presenting Cells / immunology
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Autoimmunity
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Depression, Chemical
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H-2 Antigens / genetics
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H-2 Antigens / immunology
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Immune Tolerance / drug effects*
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Interleukin-2 / genetics
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Interleukin-2 / pharmacology*
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Islets of Langerhans / immunology
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Islets of Langerhans / pathology
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Lymphocyte Activation
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Mice
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Mice, Transgenic
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Pancreatitis / congenital
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Pancreatitis / genetics
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Pancreatitis / immunology
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Pancreatitis / pathology
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T-Lymphocyte Subsets / drug effects
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T-Lymphocyte Subsets / immunology
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T-Lymphocyte Subsets / pathology
Substances
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H-2 Antigens
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H-2Kb protein, mouse
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Interleukin-2