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Harb, Hani; Stephen-Victor, Emmanuel; Crestani, Elena; Benamar, Mehdi; Massoud, Amir; Cui, Ye; Charbonnier, Louis-Marie; Arbag, Sena; Baris, Safa; Cunnigham, Amparito; Leyva-Castillo, Juan Manuel; Geha, Raif S; Mousavi, Amirhosein J; Guennewig, Boris; Schmitz-Abe, Klaus; Sioutas, Constantinos; Phipatanakul, Wanda; Chatila, Talal A
Nature immunology, 11/2020, Volume: 21, Issue: 11Journal Article
Elucidating the mechanisms that sustain asthmatic inflammation is critical for precision therapies. We found that interleukin-6- and STAT3 transcription factor-dependent upregulation of Notch4 receptor on lung tissue regulatory T (T ) cells is necessary for allergens and particulate matter pollutants to promote airway inflammation. Notch4 subverted T cells into the type 2 and type 17 helper (T 2 and T 17) effector T cells by Wnt and Hippo pathway-dependent mechanisms. Wnt activation induced growth and differentiation factor 15 expression in T cells, which activated group 2 innate lymphoid cells to provide a feed-forward mechanism for aggravated inflammation. Notch4, Wnt and Hippo were upregulated in circulating T cells of individuals with asthma as a function of disease severity, in association with reduced T cell-mediated suppression. Our studies thus identify Notch4-mediated immune tolerance subversion as a fundamental mechanism that licenses tissue inflammation in asthma.
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