Published online Sep 26, 2017. doi: 10.4252/wjsc.v9.i9.152
Peer-review started: March 31, 2017
First decision: April 18, 2017
Revised: June 21, 2017
Accepted: July 7, 2017
Article in press: July 9, 2017
Published online: September 26, 2017
Mesenchymal stromal cells (MSCs) possess great therapeutic advantages due to their ability to produce a diverse array of trophic/growth factors related to cytoprotection and immunoregulation. MSC activation via specific receptors is a crucial event for these cells to exert their immunosuppressive response. The aryl-hydrocarbon receptor (AhR) is a sensitive molecule for external signals and it is expressed in MSCs and, upon positive activation, may potentially regulate the MSC-associated immunomodulatory function. Consequently, signalling pathways linked to AhR activation can elucidate some of the molecular cascades involved in MSC-mediated immunosuppression. In this minireview, we have noted some important findings concerning MSC regulation via AhR, highlighting that its activation is associated with improvement in migration and immunoregulation, as well as an increase in pro-regenerative potential. Thus, AhR-mediated MSC activation can contribute to new perspectives on MSC-based therapies, particularly those directed at immune-associated disorders.
Core tip: The aryl-hydrocarbon receptor (AhR) is an endogenous sensor expressed in mesenchymal stromal cells (MSCs), regulating their immunomodulatory function. Therefore, in this review, we summarize important reports that demonstrate that AhR activation can substantially modulate the function of MSCs by mechanisms associated with: (1) The induction of the death signal in pro-inflammatory cells; (2) the suppression of pro-inflammatory genes/cytokines; (3) the improvement of migration and regenerative potential in acute inflammatory models; (4) the inhibition of mesodermal differentiation; and (5) the up-regulation of global immunosuppression. Thus, the influence of AhR activation on MSC function can establish new perspectives on MSC-based therapies, especially for immune-associated diseases.