B‐cell‐specific‐peroxisome proliferator‐activated receptor γ deficiency augments contact hypersensitivity with impaired regulatory B cells

Summary Nuclear receptor peroxisome proliferator‐activated receptor γ ( PPAR ‐ γ ) activation can prevent immunoinflammatory disorders and diabetes. B cells play protective roles during inflammation as well. However, the roles of endogenous PPAR ‐ γ in the regulatory properties of B cells to relieve inflammation remain unknown. Here, we developed B‐cell‐specific PPAR ‐ γ knockout (B‐ PPAR ‐ γ −/− ) mice and found that the conditional deletion of PPAR ‐ γ in B cells resulted in exaggerated contact hypersensitivity ( CHS ). Meanwhile, interferon‐ γ ( IFN ‐ γ ) of CD 4 + CD 8 + T cells was up‐regulated in B‐ PPAR ‐ γ −/− mice in CHS . This showed that the regulatory function of B cells in B‐ PPAR ‐ γ −/− mice declined in vivo . Whereas splenic CD 5 + CD 1d hi regulatory B‐cell numbers and peripheral regulatory T‐cell numbers were not changed in naive B‐ PPAR ‐ γ −/− mice. Loss of PPAR ‐ γ in B cells also did not affect either CD 86 or FasL expression in splenic CD 5 + CD 1d hi regulatory B cells after activation. Notably, interleukin‐10 ( IL ‐10) production in CD 5 + CD 1d hi regulatory B cells reduced in B‐ PPAR ‐ γ ‐deficient mice. In addition, functional IL ‐10‐producing CD 5 + CD 1d hi regulatory B cells decreased in B‐ PPAR ‐ γ −/− mice in the CHS model. These findings were in accordance with augmented CHS . The current work indicated the involvement of endogenous PPAR ‐ γ in the regulatory function of B cells by disturbing the expansion of IL ‐10‐positive regulatory B cells.