A reduction in both the severity of the disease (72, 86–98, 152, 153, 157, 158) and in the histopathology scores (88, 90, 93, 96, 158) after treatment with hMSCs was observed by the majority of studies. Furthermore, a reduction in the incidence of the disease was also reported (152). As a result, the serum level of c-telopeptide of type II collagen, a marker of cartilage degradation, was found to be decreased following hMSCs administration (86). Administration of hMSCs had an inhibitory effect in the production of pro-inflammatory cytokines such as TNF-α (72, 88, 89, 96, 97, 152, 158), IFN-γ (88, 90, 152, 158), IL-1β (89, 96, 97, 158), IL-2 (152), IL-17 (90, 152), CCL5 (152), and CXCL2 (152) and a stimulatory effect in the secretion of anti-inflammatory cytokines such as IL-5 (72), IL-10 (72, 89, 94, 96, 152, 158), and IL-13 (72). In particular, the level of IL-6, a cytokine with both pro and anti-inflammatory properties, was found to be decreased following the use of hMSCs in some studies (91, 96, 158), while in another study a higher level of IL-6 was detected after treatment with hMSCs (72). Administration of hMSCs had also a stimulatory effect in the expression of TGF-β (94, 152, 158), IDO (72, 94, 157), PGE2 (72), PDL-1 (72), and activin A (72), as demonstrated by some studies. Furthermore, in a study conducted by Gu et al. (97), a decrease in the serum levels of the inflammatory marker VEGF and the procoagulant tissue factor (TF) and an increase in the level of the anticoagulant protein antithrombin was also observed. In addition, a study conducted by Shu et al. (88) demonstrated the administration of hMSCs exerted anti-oxidative effects by significantly increasing the levels of SOD, GSH-Px, T-AOC and reducing the level of MDA. Finally, administration of hMSCs also proved to be effective in reducing the levels of autoreactive antibodies against type II collagen (86, 96, 152).