CSF2 and Crohn disease: Based on similar immune cell populations and GM-CSF effects on epithelial barrier cells in inflammatory lung and GI tract disease (e.g., influenza, aPAP, and Crohn’s disease), decreased endogenous GM-CSF leads to unopposed or dysregulated inflammation from reduced Treg and monocytic myeloid-derived suppressor cell (MDSC) numbers that dampen cytokine production, T cell proliferation, and chemotaxis; these effects damage the lungs and GI tract [27,53,57,58,59].