In addition, PKD1-insufficient mice (compared to wild-type PKD1-sufficient mice) showed significantly reduced levels of alveolitis, surface MHC-II expression on macrophages and neutrophils infiltrated into airways and interstitial lung spaces, expression of IFNγ, IL-17A, and CXCL9 in the lungs, and granuloma formation following 5-week repeated exposures to S. rectivirgula (57). This evidence concerns the gene PKD1 and hypersensitivity pneumonitis.