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Table_2_MicroRNA-31 Reduces the Motility of Proinflammatory T Helper 1 Lymphocytes.xlsx

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posted on 2018-12-06, 04:03 authored by Markus Bardua, Claudia Haftmann, Pawel Durek, Kerstin Westendorf, Antje Buttgereit, Cam Loan Tran, Mairi McGrath, Melanie Weber, Katrin Lehmann, Richard Kwasi Addo, Gitta Anne Heinz, Anna-Barbara Stittrich, Patrick Maschmeyer, Helena Radbruch, Michael Lohoff, Hyun-Dong Chang, Andreas Radbruch, Mir-Farzin Mashreghi

Proinflammatory type 1 T helper (Th1) cells are enriched in inflamed tissues and contribute to the maintenance of chronic inflammation in rheumatic diseases. Here we show that the microRNA- (miR-) 31 is upregulated in murine Th1 cells with a history of repeated reactivation and in memory Th cells isolated from the synovial fluid of patients with rheumatic joint disease. Knock-down of miR-31 resulted in the upregulation of genes associated with cytoskeletal rearrangement and motility and induced the expression of target genes involved in T cell activation, chemokine receptor– and integrin-signaling. Accordingly, inhibition of miR-31 resulted in increased migratory activity of repeatedly activated Th1 cells. The transcription factors T-bet and FOXO1 act as positive and negative regulators of T cell receptor (TCR)–mediated miR-31 expression, respectively. Taken together, our data show that a gene regulatory network involving miR-31, T-bet, and FOXO1 controls the migratory behavior of proinflammatory Th1 cells.

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