التفاصيل البيبلوغرافية
| العنوان: |
TIM-3 on myeloid cells promotes pulmonary inflammation through increased production of galectin-3 |
| المؤلفون: |
Ki Sun Kim, Chanju Lee, Hyung-Seok Kim, Su Jeong Gu, Hee Jung Yoon, Su Bin Won, Ho Lee, Yong Sun Lee, Sang Soo Kim, Lawrence P. Kane, Eun Jung Park |
| المصدر: |
Communications Biology, Vol 7, Iss 1, Pp 1-18 (2024) |
| بيانات النشر: |
Nature Portfolio, 2024. |
| سنة النشر: |
2024 |
| المجموعة: |
LCC:Biology (General) |
| مصطلحات موضوعية: |
Biology (General), QH301-705.5 |
| الوصف: |
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. |
| نوع الوثيقة: |
article |
| وصف الملف: |
electronic resource |
| اللغة: |
English |
| تدمد: |
2399-3642 |
| Relation: |
https://doaj.org/toc/2399-3642 |
| DOI: |
10.1038/s42003-024-06762-w |
| URL الوصول: |
https://doaj.org/article/53f32d3906374b9e85cb48c89f50e444 |
| رقم الانضمام: |
edsdoj.53f32d3906374b9e85cb48c89f50e444 |
| قاعدة البيانات: |
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