Poly I:C primes the suppressive function of human palatine tonsil-derived MSCs against Th17 differentiation by increasing PD-L1 expression.
It has been established that mesenchymal stem cells (MSCs) can have a suppressive effect on T cells, yet much remains unknown about the underlying mechanisms that support this effect. The T cell co-stimulatory pathway involving the programmed death-1 (PD-1) receptor and its ligand PD-L1 regulates T cell activation, tolerance, and subsequent immune-mediated tissue damage. In this study, human palatine tonsil-derived MSCs (T-MSCs) constitutively expressed PD-L1 and exhibited a suppressive activity that specifically targeted murine Th17 differentiation. Additionally, polyinosinic-polycytidylic acid (poly I:C), a Toll-like receptor 3 (TLR3) ligand, increased PD-L1 expression on T-MSCs. The elevated PD-L1 levels enhanced the suppressive functions of T-MSCs on Th17 differentiation. Therefore, pre-stimulation of T-MSCs with poly I:C may serve as an effective therapeutic priming step for modulating Th17-dominant immune responses.
['Cho|Kyung-Ah|KA|', 'Park|Minhwa|M|', 'Kim|Yu-Hee|YH|', 'Ryu|Kyung-Ha|KH|', 'Woo|So-Youn|SY|']
D060890:B7-H1 Antigen D015415:Biomarkers D002454:Cell Differentiation D005786:Gene Expression Regulation D006801:Humans D056747:Immunomodulation D016130:Immunophenotyping D008213:Lymphocyte Activation D059630:Mesenchymal Stem Cells D014066:Palatine Tonsil D011070:Poly I-C D016176:T-Lymphocyte Subsets D058504:Th17 Cells
Poly I:C Tonsil-derived MSCs Th17 PD-L1