| First Author | Subramanian S | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 2 | Pages | 1062-72 |
| PubMed ID | 16002707 | Mgi Jnum | J:100678 |
| Mgi Id | MGI:3589297 | Doi | 10.4049/jimmunol.175.2.1062 |
| Citation | Subramanian S, et al. (2005) Epistatic suppression of systemic lupus erythematosus: fine mapping of Sles1 to less than 1 mb. J Immunol 175(2):1062-72 |
| abstractText | Sle is a susceptibility locus for systemic autoimmunity derived from the lupus-prone NZM2410 mouse. The New Zealand White-derived suppressive modifier Sles1 was identified as a specific modifier of Sle1 and prevents the development of IgG anti-chromatin autoantibodies mediated by Sle1 on the C57BL/6 (B6) background. Fine mapping of Sles1 with truncated congenic intervals localizes it to a approximately 956-kb segment of mouse chromosome 17. Sles1 completely abrogates the development of activated T and B cell populations in B6.Sle1. Despite this suppression of the Sle1-mediated cell surface activation phenotypes, B6.Sle1 Sles1 splenic B cells still exhibit intrinsic ERK phosphorylation. Classic genetic complementation tests using the nonautoimmmune 129/SvJ mouse suggests that this strain possesses a Sles1 allele complementary to that of New Zealand White, as evidenced by the lack of glomerulonephritis, splenomegaly, and antinuclear autoantibody production seen in (129 x B6.Sle1 Sles1)F(1)s. These findings localize and characterize the suppressive properties of Sles1 and implicate 129 as a useful strain for aiding in the identification of this elusive epistatic modifier gene. |
