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Impaired IgE response in SWAP‐70‐deficient mice
Author(s) -
Borggrefe Tilman,
Keshavarzi Sassan,
Gross Brigitte,
Wabl Matthias,
Jessberger Rolf
Publication year - 2001
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/1521-4141(200108)31:8<2467::aid-immu2467>3.0.co;2-p
Subject(s) - biology , immunoglobulin class switching , immunoglobulin e , antibody , cd40 , wild type , mutant , microbiology and biotechnology , immunology , signal transduction , in vitro , b cell , biochemistry , cytotoxic t cell , gene
Abstract Protein SWAP‐70 was initially isolated from nuclei of activated B cells and was implicated in the immunoglobulin class switch process. After B cell activation the protein translocates from thecytoplasm to the nucleus, and may serve to signal nuclear processes. We have generated mice deficient in SWAP‐70 and found three main differences when compared to wild‐type mice: (i) their B lymphocytes are two‐ to threefold more sensitive to γ‐irradiation than B cells of wild type; (ii) SWAP‐70‐deficient mice developed autoantibodies at a much higher frequency; and (iii) the CD40 signaling pathway is compromised in the mutant mice. CD40‐dependent switching to the IgE isotype is reduced five‐ to eightfold in vitro . In SWAP‐70‐deficient mice, IgE levels prior to immunizationwere six‐ to sevenfold lower than in wild‐type mice, and after immunization three‐ to fourfold lower. CD40‐induced proliferation was transiently increased in the mutant. LPS‐induced switching to other isotypes, however, and LPS‐induced proliferation were normal. We propose that SWAP‐70 serves a specific role in the CD40 signaling pathway, in particular in the IgE response.