| First Author | Hövelmeyer N | Year | 2011 |
| Journal | Eur J Immunol | Volume | 41 |
| Issue | 3 | Pages | 595-601 |
| PubMed ID | 21341261 | Mgi Jnum | J:175422 |
| Mgi Id | MGI:5285506 | Doi | 10.1002/eji.201041313 |
| Citation | Hovelmeyer N, et al. (2011) A20 deficiency in B cells enhances B-cell proliferation and results in the development of autoantibodies. Eur J Immunol 41(3):595-601 |
| abstractText | A20/TNFAIP3 is an ubiquitin-editing enzyme, important for the regulation of the NF-kappaB 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-kappaB 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. |
