期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 41, 期 3, 页码 595-601出版社
WILEY-BLACKWELL
DOI: 10.1002/eji.201041313
关键词
Animal models; Autoimmunity; B cells; Inflammation; NF-kappa B pathway
类别
资金
- DFG [WA 1600/3-1, FOR1336, SFB/TR 52, SFB 854 (TP5), HO 4440/1-1]
- Immunology Center of Excellence Mainz (FZI)
A20/TNFAIP3 is an ubiquitin-editing enzyme, important for the regulation of the NF-kappa B pathway. Mutations in the TNFAIP3 gene have been linked to different human autoimmune disorders. In human B-cell lymphomas, the inactivation of A20 results in constitutive NF-kappa B activation. Recent studies demonstrate that in mice the germline inactivation of A20 leads to early lethality, due to inflammation in multiple organs of the body. In this report, we describe a new mouse strain allowing for the tissue-specific deletion of A20. We show that B-cell-specific deletion of A20 results in a dramatic reduction in marginal zone B cells. Furthermore, A20-deficient B cells display a hyperactive phenotype represented by enhanced proliferation upon activation. Finally, these mice develop higher levels of serum immunoglobulins, resulting in an excessive production of self-reactive autoantibodies.
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