Abstract
Five islet-reactive T cell clones were established from islet-infiltrating T cells of non-obese diabetic (NOD) mice. All clones expressed CD4, but not CD8, and responded to islet cells from various strains of mice in the context of I-ANOD. They could induce insulitis when transferred into disease-resistant I-E+ transgenic NOD mice. The T cell receptor (TCR) sequences utilized by the clones were determined. Their usage of TCR V and J segments was not restricted but was rather diverse. One of the clones utilized V beta 16. The expression of V beta 16 was significantly reduced in I-E+ transgenic NOD, suggesting the possibility that the islet-reactive T cell clone expressing V beta 16 may be deleted or inactivated by I-E molecules. This clone might be one of the candidates that triggers insulitis.
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, Differentiation, T-Lymphocyte / metabolism
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B-Lymphocytes / metabolism
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B-Lymphocytes / physiology*
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Base Sequence
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CD4 Antigens / metabolism
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CD8 Antigens
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Cells, Cultured
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Chromosome Deletion
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DNA / genetics
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Diabetes Mellitus, Experimental / genetics*
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Diabetes Mellitus, Experimental / metabolism
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Diabetes Mellitus, Experimental / physiopathology
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Female
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Gene Expression
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Genes, Recessive / genetics*
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Genes, Recessive / physiology
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Mice
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Mice, Transgenic
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Molecular Sequence Data
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Receptors, Antigen, T-Cell / genetics*
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Receptors, Antigen, T-Cell / physiology
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T-Lymphocytes / metabolism
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T-Lymphocytes / physiology*
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T-Lymphocytes / ultrastructure
Substances
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Antigens, Differentiation, T-Lymphocyte
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CD4 Antigens
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CD8 Antigens
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Receptors, Antigen, T-Cell
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DNA