MSCs are predominantly isolated from the bone marrow, adipose tissue, dental pulp, umbilical cord, Wharton’s jelly, placenta, synovial fluid, endometrium, and peripheral blood. These cells exhibit different cell-surface markers and can be used for a variety of treatment options (Table 1). MSCs can undergo in vitro amplification and self-renewal, and have low immunogenicity and immune-modulatory functions; the latter have attracted attention in clinical trials (16). MSCs have been widely used in various cellular therapies, such as pre-clinical studies, as well as in some clinical trials, because of their high safety and efficacy (17, 18). MSCs can exert immune-modu-latory effects in the host cells of both the innate and the adaptive immune system. The direct or indirect interactions of MSCs with the immune cells make the MSCs activate the immunomodulatory responses (19). The immunomodulatory functions of MSCs depend on the environment of the host cells; based on the inflammatory status, the MSCs decide the type of immunoregulatory effect (20). MSCs represent pro-inflammatory immune reactions and anti-inflammatory reactions (21). MSCs regulate the immune system via the transforming growth factor b1 (TGFβ1), which can trigger the proliferation of Tregs, induce IL-6, which prevents the proliferation of neutrophils, and stimulate the prostaglandin E2 (PGE2), which inhibits the antigen presentation by dendritic cells and proliferations of T-effector cells (22, 23). MSCs mediate these kinds of effects by direct contact, where it releases the regulatory cytokines, such as IFN-γ, indoleamine 2,3-dioxygenase, TGFβ, IL-10, and PGE2 (24). Moreover, MSCs can hinder the proliferation and/or func-tions of the CD4+ Th1 and TH17 cells, CD8+ T cells, and the natural killer (NK) cells, mainly by secreting soluble factors, such as TGFβ1 and hepatocyte growth factor (HGF) (16).