In addition, expression of and signaling through both C3aR and C5aR on nTregs has been reported to inhibit Treg function (3, 41), while pharmacological blockade of C5a has been associated with increased frequency of Tregs in a mouse GvHD model and with increased microvascular and epithelial repair in murine airway allografts (7, 24, 42). The gene discussed is C5AR1; the disease is graft versus host disease.