S1PR1 and influenza: However, previous literature has demonstrated that endothelial cells are a source of cytokines/chemokines in the lung during influenza infection, and that S1PR1 signaling in the endothelium provides a mechanism for inhibiting cytokine storms and blunting the accumulation of innate inflammatory infiltrates characterized as macrophages/monocytes, neutrophils, and NK cells3,7.