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Defective calcium-dependent signal transduction in B lymphocytes of a certain common variable immunodeficiency.

Authors
  • Kondo, N
  • Inoue, R
  • Yano, M
  • Hayashi, T
  • Miwa, Y
  • Kasahara, K
  • Yamasaki, M
  • Utsumi, M
  • Shinbara, M
  • Orii, T
Type
Published Article
Journal
Experimental and clinical immunogenetics
Publication Date
Jan 01, 1993
Volume
10
Issue
1
Pages
16–20
Identifiers
PMID: 8398198
Source
Medline
License
Unknown

Abstract

Two different common variable immunodeficiency patients were studied. Patient 1 showed hypogammaglobulinemia in all major classes of gammaglobulins and slightly reduced percentages of circulating CD19+ cells, CD20+ cells and surface IgG-or IgA-bearing cells with a normal percentage of surface IgM-bearing cells. Patient 2 showed normal levels in IgM with IgG and IgA deficiencies and almost normal percentages of circulating CD19+ cells, CD20+ cells and surface IgM-, IgG- or IgA-bearing cells. The proliferative responses of peripheral blood mononuclear cells to B cell mitogen, Staphylococcus aureus Cowan I, were reduced in patient 1 but not in patient 2. The intracellular calcium concentrations in lymphoblastoid cell lines (LCLs) transformed by Epstein-Barr virus from patient 2 were increased after anti-mu stimulation. The concentrations were scarcely increased in LCLs from patient 1. These results suggest that B cells of patient 1 have a defective Ca(2+)-dependent signal transduction pathway, resulting in a failure of cell activation and cell proliferation. The defect in B cells of patient 2 may exist on immunoglobulin gene switching or expression rather than the Ca(2+)-dependent signal transduction pathway.

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