In fibrosing alveolitis, macrophages (CD68+) and eosinophils are key sources of CCL5 [163], with CCL5 correlating with eosinophil numbers in pulmonary fibrosis caused by sulfur mustard gas inhalation [164], suggesting a potential role of CCL5 in acting on CCR3 and contributing to eosinophilia during fibrosis. This evidence concerns the gene CCR3 and pulmonary fibrosis.