| First Author | Nakajima A | Year | 2000 |
| Journal | J Autoimmun | Volume | 14 |
| Issue | 2 | Pages | 151-7 |
| PubMed ID | 10677246 | Mgi Jnum | J:60887 |
| Mgi Id | MGI:1354055 | Doi | 10.1006/jaut.1999.0356 |
| Citation | Nakajima A, et al. (2000) Treatment of lupus in NZB/W F1 mice with monoclonal antibody against Fas ligand. J Autoimmun 14(2):151-7 |
| abstractText | Since Fas ligand (FasL) can induce apoptosis of Fas-bearing cells, Fas/FasL interactions can play a critical role in maintaining self-tolerance. Fas/FasL interactions in lupus-like autoimmune disease have been well characterized in studies using either Fas or FasL mutant mice. However, the effect of the defective FasL-mediated signaling on the establishment of lupus in other mouse strains, such as NZB/W (B/W) F1, remains uncertain. In the present study, we examined the effect of anti-FasL monoclonal antibody (mAb) on the development of lupus. Treatment of B/W F1 mice with anti-FasL mAb augmented IgG1- and IgG2a-type anti-dsDNA Ab production. However, treatment of B/W F1 mice with anti-FasL mAb also significantly prevented the development of lupus nephritis. These results indicate that Fas/FasL interactions not only regulate IgG-type autoantibody production, but also influence the development of lupus nephritis in B/W F1 mice. Copyright 2000 Academic Press. |
