The combined findings for GPNMB blockade were all similar to loss of Wfdc21 function, thereby further linking immune niche–derived GPNMB to control of basal ESC reprogramming and, in turn, downstream type 2 inflammation and mucus production typical of experimental PVLD after infection with SeV or human respiratory enterovirus D68 (27, 40). This evidence concerns the gene GPNMB and infection.