CCL2 and pulmonary fibrosis: Similarly, IL-10 generates a Th2 microenvironment in favor of bleomycin- or helminth-induced lung fibrosis [91–93], which involves fibrocyte recruitment and M2 macrophage activation likely through the CCL2/CCR2 axis [94], leading to excessive extracellular matrix (ECM) deposition along with distorted lung tissue architecture, and ultimately resulting in pulmonary fibrosis and respiratory failure [95], although the underlying mechanisms are yet to be fully established.