| First Author | Borggrefe T | Year | 2001 |
| Journal | Eur J Immunol | Volume | 31 |
| Issue | 8 | Pages | 2467-75 |
| PubMed ID | 11500831 | Mgi Jnum | J:71160 |
| Mgi Id | MGI:2149250 | Doi | 10.1002/1521-4141(200108)31:8<2467::aid-immu2467>3.0.co;2-p |
| Citation | Borggrefe T, et al. (2001) Impaired IgE response in SWAP-70-deficient mice. Eur J Immunol 31(8):2467-75 |
| abstractText | 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 the cytoplasm 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 gamma-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 immunization were 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. |
