Immunodeficiency in Protein Kinase Cβ-Deficient Mice

• DOI: 10.1126/science.273.5276.788
• Publication Date: 2006-10-27T18:30:41Z
• Authors: Michael Leitges; Christian Schmedt; Rodolphe Guinamard; Jean Davoust; Stefan Schaal; Silvia Stabel; Alexander Tarakho...
• Keywords: 0301 basic medicine; B-Lymphocytes; X Chromosome; Genetic Linkage; [SDV]Life Sciences [q-bio]; T-Lymphocytes; Immunologic Deficiency Syndromes; Immunoglobulins; Receptors, Antigen, B-Cell; Protein-Tyrosine Kinases; Lymphocyte Activation; 3. Good health; [SDV] Life Sciences [q-bio]; Mice; 03 medical and health sciences; Immunoglobulin M; Immunoglobulin G; Gene Targeting; Protein Kinase C beta; Agammaglobulinaemia Tyrosine Kinase; Animals; Lymphocyte Count; Protein Kinase C; Signal Transduction

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-βI and PKC-βII 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-βI and PKC-βII play an important role in B cell activation and may be functionally linked to Bruton's tyrosine kinase in antigen receptor-mediated signal transduction.