Immunobiology of mesenchymal stem cells

Abstract

Mesenchymal stem cells (MSCs) can be isolated from almost all tissues and effectively expanded in vitro. Although their true in situ properties and biological functions remain to be elucidated, these in vitro expanded cells have been shown to possess potential to differentiate into specific cell lineages. It is speculated that MSCs in situ have important roles in tissue cellular homeostasis by replacing dead or dysfunctional cells. Recent studies have demonstrated that in vitro expanded MSCs of various origins have great capacity to modulate immune responses and change the progression of different inflammatory diseases. As tissue injuries are often accompanied by inflammation, inflammatory factors may provide cues to mobilize MSCs to tissue sites with damage. Before carrying out tissue repair functions, MSCs first prepare the microenvironment by modulating inflammatory processes and releasing various growth factors in response to the inflammation status. In this review, we focus on the crosstalk between MSCs and immune responses and their potential clinical applications, especially in inflammatory diseases.

Umbilical cord-derived stem cells (ModulatistTM) show strong immunomodulation capacity compared to adipose tissue-derived or bone marrow-derived mesenchymal stem cells

“…The results also indicate that the suppression of MSCs is associated with or mediated by PGE2, which has been previously observed for UCMSCs (Kim et al, 2015;Yu et al, 2014). However, many published publications have also suggested the role of other factors (TGFbeta, HGF, PGE 2 , NO, and IDO) in immune modulation by MSCs (Ma et al, 2014;Soleymaninejadian et al, 2012;Zhao et al, 2016).…”

Mesenchymal stem cells promote macrophage polarization toward M2b-like cells

“…4, M2b cells responded most profoundly to MSCs by shifting their cytokine production from TNF to IL-10. To determine whether an important MSC-derived immunoregulatory factor PGE-2 [26] plays a role in the modulation of M2b polarization, PGE-2 production has been inhibited in M2b-MSC cocultures (Fig. 7A).…”

Necrotic cell-derived high mobility group box 1 attracts antigen-presenting cells but inhibits hepatocyte growth factor-mediated tropism of mesenchymal stem cells for apoptotic cell death

“…Although the mechanisms are still a matter of debate, paracrine effects via secretion of a vast array of chemokines, cytokines, growth factors and other factors affecting angiogenesis, apoptosis, migration, proliferation, differentiation and extracellular matrix remodeling appear to have a central role, whereas direct tissue replacement by local engraftment and differentiation or even transdifferentiation of MSC seem uncommon. 19 In addition, MSC, 20,21 like HGF, 2 exert immunosuppressive activities, modulating DC as well as T-cell activation and function. Therefore, HGF and MSC may not only contribute to tissue regeneration after apoptotic cell death, but also to maintaining immunological tolerance.…”