For example, IL-9 knockout mice had impaired remodeling/profibrotic (M2) macrophage polarization and were protected from silica-induced fibrosis [235], whereas, chronic IL-10 exposure in mice resulted in increased pulmonary fibrosis, increased remodeling/profibrotic (M2) macrophages in BALF and in the lungs as well as increased levels of CCR2 and CCL2 [236]. The gene discussed is IL10; the disease is pulmonary fibrosis.