| First Author | Su J | Year | 2019 |
| Journal | Immunology | Volume | 156 |
| Issue | 3 | Pages | 282-296 |
| PubMed ID | 30471095 | Mgi Jnum | J:271717 |
| Mgi Id | MGI:6279112 | Doi | 10.1111/imm.13027 |
| Citation | Su J, et al. (2019) B-cell-specific-peroxisome proliferator-activated receptor gamma deficiency augments contact hypersensitivity with impaired regulatory B cells. Immunology 156(3):282-296 |
| abstractText | Nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-gamma) activation can prevent immunoinflammatory disorders and diabetes. B cells play protective roles during inflammation as well. However, the roles of endogenous PPAR-gamma in the regulatory properties of B cells to relieve inflammation remain unknown. Here, we developed B-cell-specific PPAR-gamma knockout (B-PPAR-gamma(-/-) ) mice and found that the conditional deletion of PPAR-gamma in B cells resulted in exaggerated contact hypersensitivity (CHS). Meanwhile, interferon-gamma (IFN-gamma) of CD4(+) CD8(+) T cells was up-regulated in B-PPAR-gamma(-/-) mice in CHS. This showed that the regulatory function of B cells in B-PPAR-gamma(-/-) mice declined in vivo. Whereas splenic CD5(+) CD1d(hi) regulatory B-cell numbers and peripheral regulatory T-cell numbers were not changed in naive B-PPAR-gamma(-/-) mice. Loss of PPAR-gamma in B cells also did not affect either CD86 or FasL expression in splenic CD5(+) CD1d(hi) regulatory B cells after activation. Notably, interleukin-10 (IL-10) production in CD5(+) CD1d(hi) regulatory B cells reduced in B-PPAR-gamma-deficient mice. In addition, functional IL-10-producing CD5(+) CD1d(hi) regulatory B cells decreased in B-PPAR-gamma(-/-) mice in the CHS model. These findings were in accordance with augmented CHS. The current work indicated the involvement of endogenous PPAR-gamma in the regulatory function of B cells by disturbing the expansion of IL-10-positive regulatory B cells. |
