CCR2 and pulmonary fibrosis: CCR2+ monocytes and interstitial macrophages increase in pulmonary fibrosis and produce mediators that promote fibroblast accumulation and ECM deposition, implicating a potential biomarker of inflammation in the profibrotic process [115], and the depletion of circulating monocytes using CCR2-deficient mice has resulted in profound mitigation of pulmonary fibrosis in preclinical models [116].