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 S1P2LacZ/+ 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.