Immunodeficiency in protein kinase cbeta-deficient mice

Science. 1996 Aug 9;273(5276):788-91. doi: 10.1126/science.273.5276.788.

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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Agammaglobulinaemia Tyrosine Kinase
  • Animals
  • B-Lymphocytes / immunology*
  • Gene Targeting
  • Genetic Linkage
  • Immunoglobulin G / blood
  • Immunoglobulin M / blood
  • Immunoglobulin M / immunology
  • Immunoglobulins / blood*
  • Immunologic Deficiency Syndromes / enzymology
  • Immunologic Deficiency Syndromes / immunology*
  • Lymphocyte Activation
  • Lymphocyte Count
  • Mice
  • Protein Kinase C / deficiency
  • Protein Kinase C / genetics
  • Protein Kinase C / physiology*
  • Protein Kinase C beta
  • Protein-Tyrosine Kinases / genetics
  • Protein-Tyrosine Kinases / metabolism
  • Receptors, Antigen, B-Cell / immunology
  • Signal Transduction
  • T-Lymphocytes / immunology
  • X Chromosome

Substances

  • Immunoglobulin G
  • Immunoglobulin M
  • Immunoglobulins
  • Receptors, Antigen, B-Cell
  • Protein-Tyrosine Kinases
  • Agammaglobulinaemia Tyrosine Kinase
  • Btk protein, mouse
  • Protein Kinase C
  • Protein Kinase C beta