This pathway would be consistent with a previous report in which administration of IL-2C induced fully functional Tregs that suppressed effector CD4+ T-cell proliferation and IL-5+ and IL-13+ production in airway inflammation.48 Therefore, tTreg expansion may also limit early antigen-specific and bystander type-2 responses in a number of Th2 inflammatory settings. The gene discussed is CD4; the disease is inflammatory response.