The enhanced secretion of IL-2, known for its anti-inflammatory role in SLE (51, 52), along with the decreased activation of CD154, a key target in lupus pathogenesis (53–56), could be some of the mechanisms employed by B6.Sle2c2 DCs to curtail T cell responses in cGVHD. The gene discussed is CD40LG; the disease is systemic lupus erythematosus.