Adoptive transfer of regulatory T cells can delay disease progression in a congenic murine model of SLE (130.12)

Abstract Previous studies have shown that adoptive transfer of regulatory T cells (Tregs) can prevent disease onset in murine organ-specific autoimmune disease models. Our lab studies a congenic murine model of systemic lupus erythematosus containing three susceptibility loci from the NZM2410 spontaneous model bred onto a normal B6 background, called the B6. Sle1Sle2Sle3 triple congenic strain. This strain presents with a decreased number of Tregs, yet on a per-cell basis, these Tregs are equally as capable of suppressing effector T cell (Teff) proliferation as those isolated from normal controls. To determine whether the deficiency in Treg number contributed to disease, we adoptively transferred six million isolated CD4+CD25+ Tregs or CD4+CD25− Teffs from triple congenic donors into young unmanipulated triple congenic recipients. A delay in the production of anti-nuclear antibodies as well as a decrease in spleen weight, proteinuria level, and activation of effector populations were observed four months post-transfer in those mice which received Tregs. Here we show that a single injection of unmanipulated Tregs is sufficient to ameliorate observed disease phenotypes in a systemic autoimmune disease model. This research is supported by NIH R01 AI1045050, T32 AR007603