FOXP3 and colitis: Although we could not rule out the possibility of the contribution of other factors secreted from fAT-MSCs to the FOXP3+ Treg proliferation in mice with colitis, our findings collectively suggested that fAT-MSCs inhibited inflammation by regulatory T cells via a paracrine mechanism and that PGE2 secreted by fAT-MSCs may play an important role in increasing Tregs in mice with DSS-induced colitis.