Supplementary Information 1: Characterisation of T cells and their activation from IFNγ-primed periodontal ligament cells regulate T cell responses via IFNγ-inducible mediators and ICAM-1-mediated direct cell contact

Abstract

Periodontal ligament (PDL) cells help maintain tissue homeostasis by balancing PDL tissue inflammation and regeneration. However, the mechanisms by which interferon γ (IFNγ) modulate this process are not yet fully understood. The present study aimed to examine the effect of primed and non-primed PDL cells with IFNγ on the viability and differentiation of T lymphocytes and its functional consequences. The results showed that IFNγ-primed PDL cells possessed enhanced immunosuppression by suppressing T lymphocyte viability and directing T lymphocyte differentiation towards a higher Th2/Th1 ratio. Suppression of T cell viability was mainly mediated by IFNγ-inducible secreted mediators, which was prevented in the presence of direct cell contact, likely by intercellular adhesion molecule-1 (ICAM-1)-induced PI3 K-mediated TGFβ1 expression in PDL cells. By contrast, ICAM-1 activation augmented IFNγ-induced IFNγ and IL-6 expression in PDL cells, which in turn modulated T cell differentiation. The resulting interaction between these two cell types activated macrophage and suppressed osteoclast differentiation. In conclusion, the results have shown, for the first time, that primed and non-primed PDL cells with IFNγ differentially control T cell responses via IFNγ-inducible mediators and ICAM-1-mediated direct cell contact, suggesting the role of PDL cells in shifting an inflammatory phase towards a regenerative phase