Regulatory T cell-derived IL-1Ra suppresses the innate response to respiratory viral infection.

Regulatory T (T) cell modulation of adaptive immunity and tissue homeostasis is well described; however, less is known about T cell-mediated regulation of the innate immune response. Here we show that deletion of ST2, the receptor for interleukin (IL)-33, on T cells increased granulocyte influx into the lung and increased cytokine production by innate lymphoid and γδ T cells without alteration of adaptive immunity to influenza. IL-33 induced high levels of the interleukin-1 receptor antagonist (IL-1Ra) in ST2 T cells and deletion of IL-1Ra in T cells increased granulocyte influx into the lung.