MicroRNA-142-3p Затворка в внеклеточной везиклой обозначает регуляционную дисфункцию клеток Т при множественном склерозе.
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De Rosa Giusy, Russo Claudia, Garavelli Silvia, Di Silvestre Dario, Spatocco Ilaria, Mele Giorgia, La Rocca Claudia, Colamatteo Alessandra, Carbone Fortunata, Fusco Clorinda, Passaro Fabiana, Carpi Donatella, Tagliabue Elena, Prattichizzo Francesco, Brambilla Francesca, Mauri Pierluigi, Hoxha Mirjam, Bollati Valentina, Giusti Ilaria, Dolo Vincenza, D'Antona Paola, Campomenosi Paola, Mangolini Valentina, Radeghieri Annalisa, Bergese Paolo, Morabito Ivana, Mandelli Alessandra, Finardi Annamaria, Beretta Francesca, Schilke Edoardo Dalmato, Cavaletti Guido, Dolcetti Ettore, Buttari Fabio, Abbadessa Gianmarco, Bonavita Simona, Lus Giacomo, Signoriello Elisabetta, Lanzillo Roberta, Morra Vincenzo Brescia, Mottola Maria, Zuccarelli Bruno, Uccelli Antonio, Salvetti Marco, Centonze Diego, Furlan Roberto, Matarese Giuseppe, Procaccini Claudio, de Candia Paola
Аннотация
Оригинал публикации
MicroRNA-142-3p shuttling in extracellular vesicles marks regulatory T cell dysfunction in multiple sclerosis.
CD4+CD25hiFoxP3+ regulatory T cells (Treg cells) are key controllers of immune self-tolerance, and their suppressive function is impaired in people with relapsing-remitting multiple sclerosis (pwRR-MS). Because the mechanisms underlying this condition are still ill-defined, we investigated the role of Treg cell-derived extracellular vesicles (Treg-EVs) in Treg cell dysfunction observed in pwRR-MS. We found that Treg-EVs from healthy individuals inhibit CD4+ conventional T (Tconv) cells by shuttling miR-142-3p from the Treg cell to the Tconv cell. There, miR-142-3p down-regulated mRNAs necessary for Tconv cell growth and effector functions, such as the redox controller cystine carrier SLC7A11. However, Treg cells from pwRR-MS released EVs containing reduced amounts of miR-142-3p, resulting in impaired suppressive function. Furthermore, Treg-EV miR-142-3p inversely correlated with the disability score and gadolinium-enhancing lesions in pwRR-MS. Together, our results elucidate a molecular mechanism involving miR-142-3p shuttled by Treg-EVs in the control of immune self-tolerance and unveil its pathogenetic implications in human autoimmunity.