| First Author | Brown DR | Year | 2011 |
| Journal | J Immunol | Volume | 187 |
| Issue | 1 | Pages | 21-5 |
| PubMed ID | 21622868 | Mgi Jnum | J:175934 |
| Mgi Id | MGI:5287947 | Doi | 10.4049/jimmunol.1100510 |
| Citation | Brown DR, et al. (2011) Cutting edge: an NK cell-independent role for Slamf4 in controlling humoral autoimmunity. J Immunol 187(1):21-5 |
| abstractText | Several genes within a syntenic region of human and mouse chromosome 1 are associated with predisposition to systemic lupus erythematosus. Analyses of lupus-prone congenic mice have pointed to an important role for the signaling lymphocyte activation molecule family (slamf)6 surface receptor in lupus pathogenesis. In this article, we demonstrate that a second member of the Slamf gene family, Slamf4 (Cd244), contributes to lupus-related autoimmunity. B6.Slamf4(-/-) mice spontaneously develop activated CD4 T cells and B cells and increased numbers of T follicular helper cells and a proportion develop autoantibodies to nuclear Ags. B6.Slamf4(-/-) mice also exhibit markedly increased autoantibody production in the B6.C-H-2bm12/KhEg --> B6 transfer model of lupus. Although slamf4 function is best characterized in NK cells, the enhanced humoral autoimmunity of B6.Slamf4(-/-) mice is NK cell independent, as judged by depletion studies. Taken together, our findings reveal that slamf4 has an NK cell-independent negative regulatory role in the pathogenesis of lupus a normally non-autoimmune prone genetic background. |
