| First Author | Wu XZ | Year | 2019 |
| Journal | Eur J Immunol | Volume | 49 |
| Issue | 4 | Pages | 653-665 |
| PubMed ID | 30695099 | Mgi Jnum | J:277142 |
| Mgi Id | MGI:6317146 | Doi | 10.1002/eji.201847685 |
| Citation | Wu XZ, et al. (2019) IL-10 promotes malignant pleural effusion in mice by regulating TH 1- and TH 17-cell differentiation and migration. Eur J Immunol 49(4):653-665 |
| abstractText | The role of IL-10 in malignant pleural effusion (MPE) remains unknown. By using murine MPE models, we observed that an increase in pleural IL-10 was a significant predictor of increased risk of death. We noted that TH 1- and TH 17-cell content in MPE was higher in IL-10(-/-) mice than in WT mice, and IL-10 deficiency promoted differentiation into TH 1 but not into TH 17 cells. A higher fraction of TH 1 and TH 17 cells in the MPE of IL-10(-/-) mice expressed CXCR3 compared with WT mice. We also demonstrated that Lewis lung cancer and colon adenocarcinoma cells secreted large amounts of CXCL10, a ligand of CXCR3, which induced the migration of TH 1 and TH 17 cells into the MPE, and IFN-gamma could promote this signaling cascade. Furthermore, intrapleural injection of mice with CXCL10-deficient tumor cells led to decreased TH 1- and TH 17-cell content in MPE, increased MPE volume, and reduced survival of MPE-bearing mice. Taken together, we demonstrated that IL-10 deficiency promoted T-cell differentiation into TH 1 cells and upregulated the CXCR3-CXCL10 signaling pathway that recruits TH 1 and TH 17 cells into MPE, ultimately resulting in decreased MPE formation and longer survival time of mice-bearing MPE. |
