Overexpression of TIM-3 in Macrophages Aggravates Pathogenesis of Pulmonary Fibrosis in Mice

• DOI: 10.1165/rcmb.2019-0070oc
• Publication Date: 2019-06-04T18:42:52Z
• Authors: Yu Wang; Qiyuan Kuai; Fenghua Gao; Yanbing Wang; Min He; Hong Zhou; Gencheng Han; Xingwei Jiang; Suping Ren; Qun Yu
• Keywords: Adoptive Cell Transfer; Alveolar macrophage; Pathogenesis

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disorder and lacks effective treatments because of unclear mechanisms. Aberrant function alveolar macrophages directly linked to fibrosis. Here, we show TIM-3 (T-cell immunoglobulin domain mucin domain-3), key regulator macrophage function, aggravates mRNA patients with IPF was analyzed based on the Gene Expression Omnibus Array Express databases. Lung pathology profibrotic molecules were assessed in bleomycin (BLM)-induced model using wild-type (WT) transgenic (TIM-3-TG) mice. Macrophage cells, RAW264.7, then applied investigate effect under BLM exposure vitro. depletion adoptive-transfer experiments finally performed examine morphology molecules. expression increased both our BLM-induced mouse model. TIM-3-TG mice developed more serious pathological changes tissue higher expressions TGF-β1 (transforming growth factor-β1) IL-10 than WT After treatment, significantly decreased RAW264.7 cells after knock-out, whereas it peritoneal macrophages. The scores reduced, there no difference between them depletion. Furthermore, receiving adoptive from also had those Our findings revealed that overexpressed aggravated