FIGURE 8.
Immune profile of mesenchymal stem cells (MSCs). Graphic summary of the interactions between MSC and the immune system. MSCs can suppress proliferation of both T helper (TH) and cytotoxic T cells (Tc) through multiple pathways. Differentiation of MSCs to TH2 and regulatory T-cells (Treg) is triggered, resulting in an anti-inflammatory environment. Interleukin (IL)-6 blocks the maturation of dendritic cells (DC) by inhibiting upregulation of CD40, CD80, and CD86, which subsequently reduces T-cell activation. Monocytes are stimulated by MSCs to preferentially differentiate towards the M2 phenotype. IL-10, produced by M2 macrophages, can boost the formation of Treg, and simultaneously reduces neutrophil tissue migration. Neutrophils (polymorphonuclear granulocytes; PMN) have a longer life span; however, production of reactive oxygen species (ROS) is decreased. Natural killer (NK) cell proliferation and cytotoxic activity are both suppressed. B-cell proliferation is inhibited, and production of antibodies is reduced. HGF, hepatocyte growth factor; IDO, indoleamine-pyrrole-2-3-dioxygenase; PGE2, prostaglandin E2; and TGF-β, transforming growth factor-β. (Adapted from van den Akker F, de Jager SC, Sluijter JP. Mesenchymal stem cell therapy for cardiac inflammation: iummunomodulatory properties and the influence of toll-like receptors. Mediators Inflamm 2013: 181020, 2013.)