| First Author | Wu XZ | Year | 2018 |
| Journal | Am J Physiol Lung Cell Mol Physiol | Volume | 315 |
| Issue | 3 | Pages | L443-L455 |
| PubMed ID | 29847991 | Mgi Jnum | J:265162 |
| Mgi Id | MGI:6199360 | Doi | 10.1152/ajplung.00120.2018 |
| Citation | Wu XZ, et al. (2018) Activated naive B cells promote development of malignant pleural effusion by differential regulation of TH1 and TH17 response. Am J Physiol Lung Cell Mol Physiol 315(3):L443-L455 |
| abstractText | Inflammatory signaling networks between tumor cells and immune cells contribute to the development of malignant pleural effusion (MPE). B cells have been found in MPE; however, little is known about their roles there. In the present study, by using mouse MPE models, we noted that although the total B cells in MPE were decreased as compared with the corresponding blood and spleen, the percentage of activated naive B cells expressing higher levels of CD80, CD86, myosin heavy chain-II, CD44, CD69, and programmed cell death-ligand 1 (PD-L1) molecules were increased in wild-type mouse MPE. Compared with wild-type mice, decreased T helper (TH)1 cells and increased TH17 cells were present in B cell-deficient mouse MPE, which paralleled to the reduced MPE volume and longer survival time. Adoptive transfer of activated naive B cells into B cell-deficient mice was able to increase TH1 cells and decrease TH17 cells in MPE and shorten the survival of mice bearing MPE. Furthermore, we demonstrated that activated naive B cells inhibited TH17-cell expansion via the PD-1/PD-L1 pathway and promoted naive CD4(+) T-cell differentiation into TH1/TH17 cells through secreting IL-27/IL-6 independent of the PD-1/PD-L1 pathway. Collectively, our data uncovered a mechanism by which naive B cells promote MPE formation by regulating TH1/TH17 cell responses, making these B cells an attractive target for therapeutic intervention in the fight against cancer. |
