{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T03:03:41Z","timestamp":1793243021584,"version":"4.5.0"},"reference-count":36,"publisher":"National Academy of Sciences","issue":"23","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2006,6,6]]},"abstract":"<jats:p>\n                    Atopic dermatitis (AD) is a common inflammatory skin disease of unknown etiology. Cutaneous infection with microbes such as\n                    <jats:italic>Staphylococcus aureus<\/jats:italic>\n                    and\/or skin cleansing with detergent exacerbates clinical AD. Here, we generated an AD animal model by destroying skin barrier function with detergent and subsequent topical application of protein A from\n                    <jats:italic>S. aureus<\/jats:italic>\n                    (SpA). NC\/Nga mice, which genetically have reduced skin barrier function, and BALB\/c mice having intact skin barrier function, were susceptible to this combination and developed severe and moderate AD, respectively, associated with dermal accumulation of eosinophils and mast cells. Both types of mice showed an increase in serum levels of IL-18, but not IgE. The epidermis of the NC\/Nga mice rapidly expressed T helper type 1 (Th1)-associated chemokines, including ligands for CXCR3 and CCR5, after application of both SpA and detergent, but not after application of detergent alone. Although treatment with detergent induced moderate Th1 cell response, additional SpA treatment was a prerequisite for induction of the differentiation of naive T cells toward unique Th1 cells, termed \u201csuper Th1 cells,\u201d capable of producing both Th1 (IFN-\u03b3) and T helper type 2 cytokine (IL-13), as well as IL-3, and expressing CXCR3 and CCR5. Induction of super Th1 cells required IL-18 stimulation. Blockade of IL-18 prevented AD development, whereas blockade of IL-3 partially prevented AD development, suggesting a contribution of IL-18-dependent IL-3 production to AD with cutaneous mastocytosis.\n                    <jats:italic>il18<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    BALB\/c mice similarly evaded SDS\/SpA-induced AD. Thus, IL-18 might be important for the development of infection-associated AD by induction of IL-3 from super Th1 cells.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0602900103","type":"journal-article","created":{"date-parts":[[2006,5,24]],"date-time":"2006-05-24T20:36:00Z","timestamp":1148502960000},"page":"8816-8821","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":104,"title":["Contribution of IL-18 to atopic-dermatitis-like skin inflammation induced by\n                    <i>Staphylococcus aureus<\/i>\n                    product in mice"],"prefix":"10.1073","volume":"103","author":[{"given":"Makoto","family":"Terada","sequence":"first","affiliation":[{"name":"*Division of Rheumatology and Clinical Immunology, Department of Internal Medicine, and Departments of"},{"name":"Immunology and Medical Zoology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroko","family":"Tsutsui","sequence":"additional","affiliation":[{"name":"Immunology and Medical Zoology and"},{"name":"Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Kawaguchi 332-0012, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasutomo","family":"Imai","sequence":"additional","affiliation":[{"name":"Immunology and Medical Zoology and"},{"name":"Department of Dermatology, Mie University School of Medicine, Tsu 514-8507, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koubun","family":"Yasuda","sequence":"additional","affiliation":[{"name":"Immunology and Medical Zoology and"},{"name":"Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Kawaguchi 332-0012, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hitoshi","family":"Mizutani","sequence":"additional","affiliation":[{"name":"Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Kawaguchi 332-0012, Japan;"},{"name":"Department of Dermatology, Mie University School of Medicine, Tsu 514-8507, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kiyofumi","family":"Yamanishi","sequence":"additional","affiliation":[{"name":"Dermatology, Hyogo College of Medicine, Nishinomiya 663-8501, Japan;"},{"name":"Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Kawaguchi 332-0012, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masato","family":"Kubo","sequence":"additional","affiliation":[{"name":"**Laboratory for Signal Network, RIKEN Research Center for Allergy and Immunology, RIKEN Yokohama Institute, Yokohama, Kanagawa 230-0045, 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