Idiopathic pulmonary fibrosis is a chronic and irreversible scarring disease in the lung with poor prognosis. Recently, S1P was implicated in fibrogenesis. However, the role of S1P₂ in lung fibrosis is still unknown. Here, we explored the role of S1P₂ in a murine model of lung fibrosis induced by repetitive intraperitoneal administration of BLM. S1P₂-KO mice were protected against BLM-induced lung fibrosis compared with wild-type (WT) mice. X-gal staining using S1P₂^LacZ/+ mice showed that S1P₂ is expressed in MΦs and other various constituent cells of lung and S1P₂-expressing cells accumulated in fibrotic lesion. Bone marrow chimera experiments and pharmacological inhibition of CSF1R kinase indicated the major role of MΦ S1P₂ in lung fibrosis. The gene expression analyses by DNA microarray and real-time qPCR showed that mRNA expression of Th2 cytokines and M2 markers was reduced in S1P₂-KO alveolar MΦs compared with WT alveolar MΦs. We also found impaired activation of STAT6 in S1P₂- KO alveolar MΦs. Finally, pharmacological S1P₂ blockade in WT mice alleviated BLM-induced lung fibrosis. In conclusion, S1P₂ promotes fibrogenesis by altering alveolar MΦ polarization and is a novel therapeutic target for lung fibrosis.