FcRγ Controls the Fas-Dependent Regulatory Function of Lymphoproliferative Double Negative T Cells

摘要: Patients with autoimmune lymphoproliferative syndrome (ALPS) and lymphoproliferation (LPR) mice are deficient in Fas, accumulate large numbers of αβ-TCR+, CD4−, CD8− double negative (DN) T cells. The function these DN cells remains largely unknown. common γ subunit the activating Fc receptors, FcRγ, plays an important role mediating innate immune responses. We have shown previously that a significant proportion express this molecule is required for TCR transgenic to suppress allogeneic Whether FcRγ critical LPR cell-mediated suppression responses auto allo-antigens not known. Here, we demonstrated FcRγ+, but FcRγ− could Fas+ CD4+ CD8+ cell proliferation vitro attenuated graft-versus host disease. Although expression did allow inhibit expansion Fas-deficient within context, adoptive transfer FcRγ−, inhibited generalized disease (GLD) mice. Furthermore, acted cell-intrinsic fashion limit accumulation by increasing rate apoptosis proliferated These results indicate can confer Fas-dependent regulatory properties on cells, suggest may be novel marker functional Tregs.