Differential effects of various cytokine priming on T-cell suppression and migration in canine mesenchymal stem cells.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Mesenchymal stem cells (MSCs) have been widely studied for treating immune-mediated diseases due to their immunomodulatory abilities. Recent studies have shown that priming MSCs with inflammatory cytokines can enhance these functions, yet the optimal priming conditions for canine MSCs remain poorly defined. In this study, we investigated the effects of priming canine adipose tissue-derived MSCs (cAMSCs) with inflammatory cytokines IFN-γ, TNF-α, and IL-17 at various concentrations (10, 20, and 50 ng/mL) to evaluate their immunomodulatory and migratory capacities. Of the 3 cytokines evaluated, only IFN-γ priming significantly enhanced the expression of immunosuppressive genes IDO and PD-L1, and robustly suppressed T-cell proliferation across all concentrations compared to naïve cAMSCs in both direct co-culture and indirect (conditioned medium) assays. TNF-α priming significantly increased HGF expression and promoted cell cycle progression, while IL-17 priming upregulated COX2 and TGF-β expression; however, both exhibited limited immunomodulatory effects compared to IFN-γ. In addition, IFN-γ induced strong expression of adhesion and migration-related genes, including E-CADHERIN, ICAM1, and VCAM1, and promoted cAMSCs migration in a wound healing assay. Despite increasing MHC II, IFN-γ did not induce CD80, preserving the low immunogenic profile of cAMSCs. These findings support IFN-

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.