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dc.contributor.authorSpidale, Nicholas A.
dc.contributor.authorMalhotra, Nidhi
dc.contributor.authorFrascoli, Michela
dc.contributor.authorSylvia, Katelyn E.
dc.contributor.authorMiu, Bing
dc.contributor.authorFreeman, Coral
dc.contributor.authorStadinski, Brian D.
dc.contributor.authorHuseby, Eric
dc.contributor.authorKang, Joonso
dc.date2022-08-11T08:09:55.000
dc.date.accessioned2022-08-23T16:48:59Z
dc.date.available2022-08-23T16:48:59Z
dc.date.issued2020-02-17
dc.date.submitted2020-03-11
dc.identifier.citation<p>Spidale NA, Malhotra N, Frascoli M, Sylvia K, Miu B, Freeman C, Stadinski BD, Huseby E, Kang J. Neonatal-derived IL-17 producing dermal γδ T cells are required to prevent spontaneous atopic dermatitis. Elife. 2020 Feb 17;9:e51188. doi: 10.7554/eLife.51188. PMID: 32065580; PMCID: PMC7025821. <a href="https://doi.org/10.7554/eLife.51188">Link to article on publisher's site</a></p>
dc.identifier.issn2050-084X (Linking)
dc.identifier.doi10.7554/eLife.51188
dc.identifier.pmid32065580
dc.identifier.urihttp://hdl.handle.net/20.500.14038/41372
dc.description.abstractAtopic Dermatitis (AD) is a T cell-mediated chronic skin disease and is associated with altered skin barrier integrity. Infants with mutations in genes involved in tissue barrier fitness are predisposed towards inflammatory diseases, but most do not develop or sustain the diseases, suggesting that there exist regulatory immune mechanisms to prevent aberrant inflammation. The absence of one single murine dermal cell type, the innate neonatal-derived IL-17 producing gammadelta T (Tgammadelta17) cells, from birth resulted in spontaneous, highly penetrant AD with many of the major hallmarks of human AD. In Tgammadelta17 cell-deficient mice, basal keratinocyte transcriptome was altered months in advance of AD induction. Tgammadelta17 cells respond to skin commensal bacteria and the fulminant disease in their absence was driven by skin commensal bacteria dysbiosis. AD in this model was characterized by highly expanded dermal alphabeta T clonotypes that produce the type three cytokines, IL-17 and IL-22. These results demonstrate that neonatal Tgammadelta17 cells are innate skin regulatory T cells that are critical for skin homeostasis, and that IL-17 has dual homeostatic and inflammatory function in the skin.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=32065580&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright Spidale et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectatopic dermatitis
dc.subjectbarrier autoimmunity
dc.subjectimmunology
dc.subjectinflammation
dc.subjectinterleukin-17
dc.subjectmouse
dc.subjectskin T cells
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectCongenital, Hereditary, and Neonatal Diseases and Abnormalities
dc.subjectImmune System Diseases
dc.subjectImmunity
dc.subjectImmunopathology
dc.subjectMedical Immunology
dc.subjectPathological Conditions, Signs and Symptoms
dc.subjectSkin and Connective Tissue Diseases
dc.titleNeonatal-derived IL-17 producing dermal gammadelta T cells are required to prevent spontaneous atopic dermatitis
dc.typeJournal Article
dc.source.journaltitleeLife
dc.source.volume9
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=5173&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/4154
dc.identifier.contextkey16770730
refterms.dateFOA2022-08-23T16:48:59Z
html.description.abstract<p>Atopic Dermatitis (AD) is a T cell-mediated chronic skin disease and is associated with altered skin barrier integrity. Infants with mutations in genes involved in tissue barrier fitness are predisposed towards inflammatory diseases, but most do not develop or sustain the diseases, suggesting that there exist regulatory immune mechanisms to prevent aberrant inflammation. The absence of one single murine dermal cell type, the innate neonatal-derived IL-17 producing gammadelta T (Tgammadelta17) cells, from birth resulted in spontaneous, highly penetrant AD with many of the major hallmarks of human AD. In Tgammadelta17 cell-deficient mice, basal keratinocyte transcriptome was altered months in advance of AD induction. Tgammadelta17 cells respond to skin commensal bacteria and the fulminant disease in their absence was driven by skin commensal bacteria dysbiosis. AD in this model was characterized by highly expanded dermal alphabeta T clonotypes that produce the type three cytokines, IL-17 and IL-22. These results demonstrate that neonatal Tgammadelta17 cells are innate skin regulatory T cells that are critical for skin homeostasis, and that IL-17 has dual homeostatic and inflammatory function in the skin.</p>
dc.identifier.submissionpathoapubs/4154
dc.contributor.departmentDepartment of Pathology
dc.source.pagese51188


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Copyright Spidale et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
Except where otherwise noted, this item's license is described as Copyright Spidale et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.