Injury, dysbiosis and filaggrin deficiency drive skin inflammation via keratinocyte IL-1α release

Our data demonstrate that injury and dysbiosis drive intracellular IL-1α release from keratinocytes to mediate chronic inflammation in filaggrin-deficient mice. IL-1α and dysbiosis could represent therapeutic targets to reduce skin inflammation in atopic dermatitis.

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Bibliographic Details
Published inJournal of allergy and clinical immunology Vol. 143; no. 4; pp. 1426 - 1443.e6
Main Authors Archer, Nathan K., Jo, Jay-Hyun, Lee, Steven K., Kim, Dongwon, Smith, Barbara, Ortines, Roger V., Wang, Yu, Marchitto, Mark C., Ravipati, Advaitaa, Cai, Shuting S., Dillen, Carly A., Liu, Haiyun, Miller, Robert J., Ashbaugh, Alyssa G., Uppal, Angad S., Oyoshi, Michiko, Malhotra, Nidhi, Hoff, Sabine, Garza, Luis A, Kong, Heidi H., Segre, Julia A., Geha, Raif S., Miller, Lloyd S.
Format Journal Article
LanguageEnglish
Published 19.09.2018
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Summary:Our data demonstrate that injury and dysbiosis drive intracellular IL-1α release from keratinocytes to mediate chronic inflammation in filaggrin-deficient mice. IL-1α and dysbiosis could represent therapeutic targets to reduce skin inflammation in atopic dermatitis.
Bibliography:Author contributions: N.K.A., L.A.G., H.H.K., J.A.S., R.S.G. and L.S.M. designed research; N.K.A., J-H.J., S.K.L., D.K., B.S., R.V.O., Y.W., M.C.M., A.R., S.S.C., C.A.D., H.L., R.J.M., A.G.A., A.S.U., M.O., N.M. and S.H. performed research; L.A.G., J-H.J., H.H.K., J.A.S., R.S.G. contributed new reagents/analytic tools; N.K.A., J-H.J., L.A.G., H.H.K., J.A.S., R.S.G. and L.S.M. analyzed data; and N.K.A., H.H.K., J.A.S., R.S.G. and L.S.M. wrote the paper.
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ISSN:0091-6749
1097-6825
DOI:10.1016/j.jaci.2018.08.042