| First Author | Schwarting A | Year | 2005 |
| Journal | J Am Soc Nephrol | Volume | 16 |
| Issue | 11 | Pages | 3264-72 |
| PubMed ID | 16221871 | Mgi Jnum | J:116824 |
| Mgi Id | MGI:3695079 | Doi | 10.1681/ASN.2004111014 |
| Citation | Schwarting A, et al. (2005) Interferon-beta: a therapeutic for autoimmune lupus in MRL-Faslpr mice. J Am Soc Nephrol 16(11):3264-72 |
| abstractText | Type I interferons are associated with lupus. Genes that are regulated by IFN-alpha are upregulated in pediatric lupus patients. Gene deletion of the IFN-alpha/beta receptor in experimental lupus-like NZB mice results in reduced disease activity. Conversely, IFN-beta is a well-established treatment in multiple sclerosis, another autoimmune disease. For determining whether IFN-beta treatment is harmful or beneficial in lupus, MRL-Fas(lpr) mice were injected with this type I IFN. Treatment was initiated in MRL-Fas(lpr) mice with mild and advanced disease. IFN-beta was highly effective in prolonging survival and ameliorating the clinical (renal function, proteinuria, splenomegaly, and skin lesions), serologic (autoantibodies and cytokines), and histologic parameters of the lupus-like disease in mice that had mild and advanced disease. Several underlying mechanisms of IFN-beta therapy involving cellular (decreased T cell proliferation and infiltration of leukocytes into the kidney) and humoral (decrease in IgG3 isotypes) immune responses and a reduction in nephrogenic cytokines were identified. In conclusion, IFN-beta treatment of lupus nephritis in MRL-Fas(lpr) mice is remarkably beneficial and suggests that IFN-beta may be an appealing therapeutic candidate for subtypes of human lupus. |
