Enhancement of fibrosis development in VD3-deficient mice with developing HP was strongly associated with an increased influx of immune cells into the lungs (especially neutrophils, macrophages, dendritic cells and lymphocytes Tc), disturbed release of several cytokines (lowered amount of IL1β, IL6, IL12, IL4 IL10, IL13), intensified production of growth factors favouring fibrosis response (FGF2 and TGFβ), and, most important of all, accelerated EMT underlying fibrosis (over-expression of EMT-transcription factors and mesenchymal cell markers). This evidence concerns the gene IL1B and hypersensitivity pneumonitis.