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Idiopathic pulmonary fibrosis is a chronic, progressive, and irreversible fibrotic lung disease. Although inflammation plays a central role in the pathogenesis of idiopathic pulmonary fibrosis, how inflammatory responses are regulated remains unclear. In this article, we show that mice deficient in the immunoreceptor CD300c2 (also called MAIR-II, LMIR2, and CLM-4) showed longer survival; less collagen deposition in the lung; lower levels of neutrophil chemoattractants, such as TNF-α, CXCL1, and CCL2; and fewer neutrophils in the bronchoalveolar fluid than wild-type mice after intratracheal administration of bleomycin (BLM). We also found that BLM administration induced the release of the danger-associated molecular pattern HMGB-1, which caused CD300c2-deficient alveolar macrophages, via TLR4, to produce lower levels of neutrophil chemoattractants than wild-type alveolar macrophages. Our findings demonstrate that CD300c2 contributes to BLM-induced inflammatory responses mediated by alveolar macrophages.

Cutting Edge: Involvement of the Immunoreceptor CD300c2 on Alveolar Macrophages in Bleomycin-Induced Lung Fibrosis