A novel isoform of the Ly108 gene ameliorates murine lupus Keszei, Marton Detre, Cynthia Rietdijk, Svend Muñoz Fernández, Pilar Romero, Xavier Berger, Scott B Calpe, Silvia Liao, Gongxian Castro, Wilson Julien, Aimee Wu, Ying-Yu Shin, Dong-Mi Sancho, Jaime Zubiaur, Mercedes Herbert C. Morse III Morel, Laurence Engel, Pablo Wang, Ninghai Terhorst, Cox Studies of human systemic lupus erythematosus patients and of murine congenic mouse strains associate genes in a DNA segment on chromosome 1 with a genetic predisposition for this disease. The systematic analysis of lupus-prone congenic mouse strains suggests a role for two isoforms of the Ly108 receptor in the pathogenesis of the disease. In this study, we demonstrate that Ly108 is involved in the pathogenesis of lupus-related autoimmunity in mice. More importantly, we identified a third protein isoform, Ly108-H1, which is absent in two lupus-prone congenic animals. Introduction of an Ly108-H1– expressing transgene markedly diminishes T cell–dependent autoimmunity in congenic B6.Sle1b mice. Thus, an immune response–suppressing isoform of Ly108 can regulate the pathogenesis of lupus. 2025-01-16T08:42:29Z 2025-01-16T08:42:29Z 2011 journal article https://hdl.handle.net/10481/99329 http://creativecommons.org/licenses/by-nc-nd/4.0/ open access Attribution-NonCommercial-NoDerivatives 4.0 Internacional