Purpose: To examine the effect of peroxisome proliferator activated receptor-γ(PPARγ) ligand, 15d-PGJ2 on inhibition of T cell proliferation and T cell-mediated osteoclastogenesis, and clarify the possible mechanism.
Methods: T cells from A.actinomycetetemcomitans immunized BALB/c mice were isolated from cervical lymph nodes and T lymphocytes enriched in vitro. At 3-day after 15d-PGJ2 (0,1×10(-8),1×10(-7),1×10(-6),1×10(-5)mol/L) induction,T cell proliferation analysis was measured by cintilography, the concentration of RANKL, TNF-α and IL-10 were measured in culture supernatants by ELISA, and osteoclastogenesis of co-culture with RAW 264.7 cell and T lymphocyte supernatants that enriched in vitro by tartrate resistant acid phosphatase (TRAP) staining. SASS 11.0 software package was used for statistical analysis.
Results: By 1×10-5mol/L 15d-PGJ2 induction, T cell 3H incorporation remarkably decreased, the expression of RANKL and TNF-α in the supernatant markedly decreased, significantly different compared with the control group(P<0.05), but IL-10 was not significantly different, and the numbers of TRAP positive cells decreased, significantly different compared with the control group (P<0.05),which was dose-dependent.
Conclusions: PPARγ ligand 15d-PGJ2 can inhibit 3H incorporation, down-regulate cytokine release, decrease T cell-induced osteoclastogenesis. The data suggest that PPARγ ligand plays an important role in T cell-induced bone resorption.