Background
Rheumatoid arthritis (RA) is a chronic, progressive, and inflammatory autoimmune disease which primarily affects the small arthrodial joints. The
Conclusions
GMSC-based therapy induces T-cell apoptosis via the FasL/Fas pathway and results in immune tolerance and amelioration of the CIA inflammation.
Methods
DBA/1 mice with collagen II-induced arthritis were treated with GMSCs from the C57BL/6 J mouse, the B6Smn.C3-FasLgld/J mouse (FasL-/- GMSCs), and FasL overexpressed FasL-/- GMSCs (FasL TF GMSCs). Inflammation was evaluated by measuring clinical score, tumor necrosis factor (TNF)-α and anti-collagen II antibody levels, and histological analyses. The levels of CD4+ Th cell subsets in spleens and draining lymph nodes were assessed by flow cytometric analysis.
Results
Systemic infusion of GMSCs can significantly reduce the severity of experimental arthritis, and resume the balance of Th cell subsets. FasL-/- GMSCs failed to induce apoptosis of activated T cells in vitro and in vivo, and therefore show no therapeutic effects, whereas FasL TF GMSCs can rescue the immunosuppressant effects in the treatment of CIA. Conclusions: GMSC-based therapy induces T-cell apoptosis via the FasL/Fas pathway and results in immune tolerance and amelioration of the CIA inflammation.