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Pro-inflammatory T cells and Mesenchymal Stem Cells (MSCs) represent a critical cellular interaction system involved in the regulation of the adaptive immune response. MSCs are multipotent progenitor cells that exhibit significant immunomodulatory properties, particularly their ability to inhibit the activation, differentiation, and proliferation of pro-inflammatory T cell subsets, including Th1 and Th17 cells (Gao et al., 2016). This interaction is primarily mediated by the secretion of immunosuppressive factors such as indoleamine 2,3-dioxygenase (IDO), prostaglandin E2 (PGE2), and transforming growth factor-beta (TGF-beta), as well as through direct cell-surface molecule interactions (Wang et al., 2014). In the presence of inflammatory cytokines like IFN-gamma and TNF-alpha, MSCs become licensed to suppress T cell-mediated inflammation, promoting a shift toward a more regulatory immune environment (Bernardo & Fibbe, 2013). This cellular crosstalk is a major focus of cell-based therapies for treating immune-mediated conditions such as graft-versus-host disease (GvHD), Crohn's disease, and rheumatoid arthritis. Understanding this relationship is essential for developing effective MSC-based therapeutics and monitoring their efficacy in clinical settings.
MSCs suppress pro-inflammatory T cells through the secretion of soluble factors (IDO, PGE2, TGF-beta, IL-10) and direct cell-to-cell contact, leading to cell cycle arrest and induction of regulatory T cells.
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