ERK phosphorylation and miR-181a expression modulate activation of human memory TH17 cells

Federico Mele, Camilla Basso, Cristina Leoni, Dominik Aschenbrenner, Simone Becattini, Daniela Latorre, Antonio Lanzavecchia, Federica Sallusto () and Silvia Monticelli ()
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Federico Mele: Institute for Research in Biomedicine, Università della Svizzera italiana
Camilla Basso: Institute for Research in Biomedicine, Università della Svizzera italiana
Cristina Leoni: Institute for Research in Biomedicine, Università della Svizzera italiana
Dominik Aschenbrenner: Institute for Research in Biomedicine, Università della Svizzera italiana
Simone Becattini: Institute for Research in Biomedicine, Università della Svizzera italiana
Daniela Latorre: Institute for Research in Biomedicine, Università della Svizzera italiana
Antonio Lanzavecchia: Institute for Research in Biomedicine, Università della Svizzera italiana
Federica Sallusto: Institute for Research in Biomedicine, Università della Svizzera italiana
Silvia Monticelli: Institute for Research in Biomedicine, Università della Svizzera italiana

Nature Communications, 2015, vol. 6, issue 1, 1-12

Abstract: Abstract T helper (TH) cell polarization during priming is modulated by a number of signals, but whether polarization to a given phenotype also influences recall responses of memory TH cells is relatively unknown. Here we show that miR-181a is selectively induced in both human and mouse naive T cells differentiating into the TH17, but not TH1 or TH2 subset. In human memory TH17 cells, miR-181a regulates responses to cognate antigens through modulation of ERK phosphorylation. By enhancing the signalling cascade from the T-cell receptor, such molecular network reduces the threshold of TH17 cell activation. Moreover, at a late time point, the same network induces a self-regulatory mechanism dependent on ID3, a negative regulator of transcription factors that control RORC expression, thus modulating TH17 activity. Our results demonstrate that the phenotype acquired by TH cells during priming contributes to their threshold of activation to secondary antigenic stimulations, thus influencing memory responses.

Date: 2015
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DOI: 10.1038/ncomms7431

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