| First Author | Braun D | Year | 2003 |
| Journal | J Autoimmun | Volume | 20 |
| Issue | 1 | Pages | 15-25 |
| PubMed ID | 12604309 | Mgi Jnum | J:82338 |
| Mgi Id | MGI:2652307 | Doi | 10.1016/s0896-8411(02)00109-9 |
| Citation | Braun D, et al. (2003) Type I Interferon controls the onset and severity of autoimmune manifestations in lpr mice. J Autoimmun 20(1):15-25 |
| abstractText | Type I Interferons (IFN-I) are immunoregulatory cytokines that enhance activation and survival of many cellular components of the immune system. In the present work, we evaluated the effect of IFN-I on the development of the lymphoproliferative disorder in Fas-defective lpr mice. We report that sustained injection of polyinosinic:polycytidylic acid, a potent inducer of IFN-I, in B6 lpr mice resulted in a dramatic aggravation of the renal disease, higher titers of autoantibodies, a 10-fold increase in serum Ig and accumulation of activated lymphocytes. Moreover, introducing a null mutation for the IFN-I-Receptor gene into the lpr background resulted in dramatic decrease of immune complexes deposition in the kidney and reduced lymphadenopathy. While several recent reports correlated serum levels of IFN-alpha with disease activity in systemic Lupus erythematosus patients, our findings establish a causal link from IFN-I production to the onset and severity of another related autoimmune syndrome. |
