TIM-3 on myeloid cells promotes pulmonary inflammation through increased production of galectin-3.

ABSTRACT: T cell immunoglobulin and mucin-containing molecule 3 (TIM-3) exhibits unique, cell type- and context-dependent characteristics and functions. Here, we report that TIM-3 on myeloid cells plays essential roles in modulating lung inflammation. We found that myeloid cell-specific TIM-3 knock-in (FSF-TIM3/LysM-Cre⁺) mice have lower body weight and shorter lifespan than WT mice. Intriguingly, the lungs of FSF-TIM3/LysM-Cre⁺ mice display excessive inflammation and features of disease-associated pathology. We further revealed that galectin-3 levels are notably elevated in TIM-3-overexpressing lung-derived myeloid cells. Furthermore, both TIM-3 blockade and GB1107, a galectin-3 inhibitor, ameliorated lung inflammation in FSF-TIM3/LysM-Cre^+/- mice. Using an LPS-indu

SUBMITTER: Kim KS 

PROVIDER: S-EPMC11377825 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature