Abstract
Cross-linking of the antigen receptor on lymphocytes by antigens or antibodies to the receptor results in activation of enzymes of the protein kinase C (PKC) family. Mice homozygous for a targeted disruption of the gene encoding the PKC-betaI and PKC-betaII isoforms develop an immunodeficiency characterized by impaired humoral immune responses and reduced cellular responses of B cells, which is similar to X-linked immunodeficiency in mice. Thus PKC-betaI and PKC-betaII play an important role in B cell activation and may be functionally linked to Bruton's tyrosine kinase in antigen receptor-mediated signal transduction.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Agammaglobulinaemia Tyrosine Kinase
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Animals
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B-Lymphocytes / immunology*
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Gene Targeting
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Genetic Linkage
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Immunoglobulin G / blood
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Immunoglobulin M / blood
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Immunoglobulin M / immunology
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Immunoglobulins / blood*
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Immunologic Deficiency Syndromes / enzymology
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Immunologic Deficiency Syndromes / immunology*
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Lymphocyte Activation
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Lymphocyte Count
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Mice
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Protein Kinase C / deficiency
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Protein Kinase C / genetics
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Protein Kinase C / physiology*
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Protein Kinase C beta
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Protein-Tyrosine Kinases / genetics
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Protein-Tyrosine Kinases / metabolism
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Receptors, Antigen, B-Cell / immunology
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Signal Transduction
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T-Lymphocytes / immunology
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X Chromosome
Substances
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Immunoglobulin G
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Immunoglobulin M
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Immunoglobulins
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Receptors, Antigen, B-Cell
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Protein-Tyrosine Kinases
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Agammaglobulinaemia Tyrosine Kinase
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Btk protein, mouse
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Protein Kinase C
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Protein Kinase C beta