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

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

  • Commun Biol. 2024 Sep 5;7(1):1090. doi: 10.1038/s42003-024-06762-w.
Ki Sun Kim 1,  Chanju Lee 1 2,  Hyung-Seok Kim 1,  Su Jeong Gu 1,  Hee Jung Yoon 2,  Su Bin Won 1 2,  Ho Lee 1,  Yong Sun Lee 1,  Sang Soo Kim 3,  Lawrence P Kane 4,  Eun Jung Park 5 6
Affiliations

Affiliations

  • 1 Department of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang-si, Gyeonggi-do, 10408, Republic of Korea.
  • 2 Immuno-oncology Branch, National Cancer Center, Goyang-si, Gyeonggi-do, 10408, Republic of Korea.
  • 3 Radiological Science Branch, National Cancer Center, Goyang-si, Gyeonggi-do, 10408, Republic of Korea.
  • 4 Department of Immunology, University of Pittsburgh, Pittsburgh, PA, 15213, USA.
  • 5 Department of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang-si, Gyeonggi-do, 10408, Republic of Korea. ejpark@ncc.re.kr.
  • 6 Immuno-oncology Branch, National Cancer Center, Goyang-si, Gyeonggi-do, 10408, Republic of Korea. ejpark@ncc.re.kr.
PMID: 39237613 DOI: 10.1038/s42003-024-06762-w
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-induced lung inflammation model with myeloid cell-specific TIM-3 knock-out mice, we demonstrated the association of TIM-3 with both lung inflammation and Galectin-3. Collectively, our findings suggest that myeloid TIM-3 is an important regulator in the lungs and that modulation of TIM-3 and Galectin-3 could offer therapeutic benefits for inflammation-associated lung diseases.

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Products
  • Cat. No.
    Product Name
    Description
    Target
    Research Area
  • HY-114409
    99.92%, Galectin-3 Inhibitor