IL23A and pulmonary fibrosis: This study characterized the role of innate immune responses in lung fibrosis using 11 individual knock out mouse models lacking different members of IL-1 family including, ASC, NALP3, IL-1R, IL-18R, ILK-33R, IL-1a and IL-1b, as well as other innate immune response mediators such as MyD88, TLR2/4, TLR3, TRIF, IL-23p19, and TCRδ.