Abstract
The LAG3 protein has several features in common with CD4, suggesting that it may be important in controlling T cell reactivity. However, mice with a Lag3 null mutation have now been shown to exhibit a defect in the natural killer cell, rather than the T cell, compartment. Killing of certain tumor targets by natural killer cells from these mice was inhibited or even abolished, whereas lysis of cells displaying major histocompatibility complex class I disparities remained intact. It appears that LAG3 is a receptor or coreceptor that defines different modes of natural killing.
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*
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B-Lymphocytes / immunology
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Base Sequence
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Cytotoxicity, Immunologic*
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Female
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Histocompatibility Antigens Class I / immunology
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Killer Cells, Natural / immunology*
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Lymphocyte Activation Gene 3 Protein
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Male
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Membrane Proteins / genetics
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Membrane Proteins / physiology*
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Mice
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Mice, Inbred C57BL
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Molecular Sequence Data
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Mutation
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Phenotype
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T-Lymphocytes / immunology
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Tumor Cells, Cultured
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beta 2-Microglobulin / deficiency
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beta 2-Microglobulin / physiology
Substances
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Antigens, CD
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Histocompatibility Antigens Class I
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Membrane Proteins
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beta 2-Microglobulin
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Lymphocyte Activation Gene 3 Protein
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Lag3 protein, mouse