Abstract
Immune system disorders, especially Tcell disorders, are important therapeutic targets of mesenchymal stem cells (MSCs) in many autoimmune diseases (ADs). Although extracellular regulated protein kinases (ERKs) play a role in MSC therapy by promoting Tcell apoptosis, the mechanism remains unclear. Our findings indicate that ERK1-/- bone marrow MSCs (BMMSCs), but not ERK2-/- BMMSCs, failed to promote Tcell apoptosis due to incapacity to activate the ETS2/AURKA/NF-κB/Fas/MCP-1 cascade. Moreover, ERK1-/- BMMSCs were unable to upregulate regulatory Tcells and suppress T helper 17 cells. Licochalcone A (LA), which promotes ERK pathway activation, enhanced the therapeutic efficacy of MSC therapy in ulcerative colitis and collagen-induced arthritis mice. Our findings suggest that ERK1, but not ERK2, plays a crucial role in regulating Tcells in MSCs. LA-treated MSCs provide a strategy to improve the efficacy of MSC-based treatments for ADs.
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