Abstract
LAT (linker for activation of T cells) is essential for T cell receptor signaling. Mice homozygous for a mutation of the three C-terminal LAT tyrosine residues showed a block in alphabeta T cell development and a partially impaired gammadelta T cell development. Without intentional immunization, they accumulated gammadelta T cells in the spleen and lymph nodes that chronically produced T helper type 2 cytokines in large amounts, and caused the maturation of plasma cells secreting immunoglobulin E (IgE) and IgG1. These effects are very similar to that triggered in the alphabeta lineage by a mutation involving a distinct LAT tyrosine. Thus, LAT is an essential regulator of T cell homeostasis and terminal differentiation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing*
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Animals
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Base Sequence
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Carrier Proteins / genetics
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Carrier Proteins / immunology*
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Cell Differentiation / genetics
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Cell Differentiation / immunology
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Cytokines / immunology
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Flow Cytometry
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Homeostasis / immunology
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Immunohistochemistry
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Lymphocyte Activation / immunology
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Membrane Proteins*
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Mice
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Mice, Inbred BALB C
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Mice, Knockout
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Molecular Sequence Data
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Mutation
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Phenotype
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Phosphoproteins / genetics
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Phosphoproteins / immunology*
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Receptors, Antigen, T-Cell, gamma-delta / genetics
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Receptors, Antigen, T-Cell, gamma-delta / immunology*
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Signal Transduction / genetics
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Signal Transduction / immunology
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Spleen / immunology
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T-Lymphocytes / immunology*
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Th2 Cells / immunology
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Th2 Cells / metabolism
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Tyrosine / genetics
Substances
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Adaptor Proteins, Signal Transducing
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Carrier Proteins
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Cytokines
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Lat protein, mouse
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Membrane Proteins
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Phosphoproteins
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Receptors, Antigen, T-Cell, gamma-delta
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Tyrosine