ArticleFrontiers in immunology2026
Immunomodulatory properties of human dental pulp stromal cells: the role of IL-6/JAK/STAT3 pathway and PD-L1.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Multi-omics mapping of PSC genetic risk to a high TWAS-active JAML+ lipid-associated macrophage program: bridging single-cell heterogeneity, spatial fibrotic niches, and machine learning selection.Frontiers in cell and developmental biology · 2026Article
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13 authors.
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Abstract
Introduction: Human Dental Pulp Stromal Cells (hDPSCs) of neural-ectodermal origin hold immunomodulatory properties which make them a source for MSC-based therapies for the treatment of autoimmune diseases. Methods: In this study hDPSCs were exposed to inflammatory conditions mimicked by co-culture with Peripheral Blood Mononuclear Cells activated with anti-CD3/CD28 (aPBMCs) or treatment with Conditioned Medium (CM) from aPBMCs with or without the addition of a specific IL6 receptor (IL6R) inhibitor. To assess IL-6 effects on PD-L1 expression, hDPSCs were treated with IL-6/sIL6R complex and the activation of IL-6 trans-signalling was investigated. The functional role of IL-6 in modulating PD-L1 protein stability was further confirmed by treating hDPSCs with a proteasome inhibitor. Results: Our results highlighted that hDPSCs exposed to different inflammatory conditions activate Fas/FasL and PD1/PD-L1 pathways. Moreover, hDPSCs modulate inflammatory cytokines release of aPBMCs from Rheumatoid Arthritis (RA) patients. However, the inflammatory milieu induced the upregulation of IL-6 by hDPSCs, which was demonstrated to be strongly correlated to PD-L1 expression, suggesting its involvement in supporting their immunoregulation. Our data demonstrated that the activation of the IL6/JAK/STAT3 trans-signaling pathway in hDPSCs through stimulation with the IL6/sIL6R complex leads to an increase in PD-L1 protein levels, but not PD-L2, via proteasome inhibition. Conclusion: Our study demonstrates the activation of the IL-6/PD-L1 axis in response to inflammatory conditions and underscores its potential significance in autoimmune diseases since a dysfunction of this mechanism could lead to the onset and progression of chronic inflammatory disorders.
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