@article {542221, title = {Cutting edge: an NK cell-independent role for Slamf4 in controlling humoral autoimmunity.}, journal = {J Immunol}, volume = {187}, number = {1}, year = {2011}, month = {2011 Jul 1}, pages = {21-5}, abstract = {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 {\textrightarrow} 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.}, keywords = {Animals, Antigens, CD, Autoantibodies, Chromatin, Chronic Disease, Disease Models, Animal, Genetic Predisposition to Disease, Graft vs Host Disease, Humans, Immune Tolerance, Killer Cells, Natural, Lupus Erythematosus, Systemic, Mice, Mice, Inbred C57BL, Mice, Knockout, Receptors, Immunologic}, issn = {1550-6606}, doi = {10.4049/jimmunol.1100510}, author = {Brown, Daniel R and Calpe, Silvia and Keszei, Marton and Wang, Ninghai and McArdel, Shannon and Terhorst, Cox and Sharpe, Arlene H} }