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Genome sequence comparisons between\n              <jats:italic>S. argenteus<\/jats:italic>\n              isolates and representative\n              <jats:italic>S. aureus<\/jats:italic>\n              clinical isolates from various origins revealed that the\n              <jats:italic>S. argenteus<\/jats:italic>\n              genome from AD patients closely resembles that of\n              <jats:italic>S. aureus<\/jats:italic>\n              causing skin infections. We previously reported that 17%\u201322% of\n              <jats:italic>S. aureus<\/jats:italic>\n              isolated from skin infections produce staphylococcal enterotoxin Y (SEY), which predominantly induces T-cell proliferation via the T-cell receptor (TCR) V\u03b1 pathway. Complete genome sequencing of\n              <jats:italic>S. argenteus<\/jats:italic>\n              isolates revealed a gene encoding a protein similar to superantigen SEY, designated as SargEY, on its chromosome. Population structure analysis of\n              <jats:italic>S. argenteus<\/jats:italic>\n              revealed that these isolates are ST2250 lineage, which was the only lineage positive for the SEY-like gene among\n              <jats:italic>S. argenteus<\/jats:italic>\n              . Recombinant SargEY demonstrated immunological cross-reactivity with anti-SEY serum. SargEY could induce proliferation of human CD4\n              <jats:sup>+<\/jats:sup>\n              and CD8\n              <jats:sup>+<\/jats:sup>\n              T cells, as well as production of TNF-\u03b1 and IFN-\u03b3. SargEY showed emetic activity in a marmoset monkey model. S\n              <jats:sub>arg<\/jats:sub>\n              EY and SET (a phylogenetically close but uncharacterized SE) revealed their dependency on TCR V\u03b1 in inducing human T-cell proliferation. Additionally, TCR sequencing revealed other previously undescribed V\u03b1 repertoires induced by SEH. S\n              <jats:sub>arg<\/jats:sub>\n              EY and SEY may play roles in exacerbating the respective toxin-producing strains in AD.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>IMPORTANCE<\/jats:title>\n            <jats:p>\n              <jats:italic>Staphylococcus aureus<\/jats:italic>\n              is frequently isolated from active lesions of atopic dermatitis (AD) patients. We reported that 17%\u201322% of\n              <jats:italic>S. aureus<\/jats:italic>\n              isolated from AD patients produced a novel superantigen staphylococcal enterotoxin Y (SEY). Unlike many\n              <jats:italic>S<\/jats:italic>\n              .\n              <jats:italic>aureus<\/jats:italic>\n              superantigens that activate T cells via T-cell receptor (TCR) V\u00df, SEY activates T cells via TCR V\u03b1 and stimulates cytokine secretion.\n              <jats:italic>Staphylococcus argenteus<\/jats:italic>\n              was isolated from AD patients during the surveillance for\n              <jats:italic>S. aureus<\/jats:italic>\n              . Phylogenetic comparison of the genome indicated that the isolate was very similar to\n              <jats:italic>S. aureus<\/jats:italic>\n              causing skin infections. The isolate encoded a SEY-like protein, designated SargEY, which, like SEY, activated T cells via the TCR V\u03b1. ST2250 is the only lineage positive for SargEY gene. ST2250\n              <jats:italic>S. argenteus<\/jats:italic>\n              harboring a superantigen SargEY gene may be a novel staphylococcal clone that infects human skin and is involved in the exacerbation of AD.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/msphere.00505-24","type":"journal-article","created":{"date-parts":[[2024,7,11]],"date-time":"2024-07-11T13:21:43Z","timestamp":1720704103000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":4,"title":["Genomic analysis and identification of a novel superantigen, SargEY, in\n            <i>Staphylococcus argenteus<\/i>\n            isolated from atopic dermatitis lesions"],"prefix":"10.1128","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0831-914X","authenticated-orcid":false,"given":"Fatkhanuddin","family":"Aziz","sequence":"first","affiliation":[{"name":"Department of Bacteriology, Graduate School of Biomedical and Health Sciences, Hiroshima City, Hiroshima, Japan"},{"name":"Veterinary Technology Program, Department of Bioresources Technology and Veterinary, Vocational College, Universitas Gadjah Mada, Yogyakarta, Indonesia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9330-4203","authenticated-orcid":false,"given":"Junzo","family":"Hisatsune","sequence":"additional","affiliation":[{"name":"Department of Bacteriology, Graduate School of Biomedical and Health Sciences, Hiroshima City, Hiroshima, Japan"},{"name":"Antimicrobial Resistance Research Center, National Institute of Infectious Diseases, Higashimurayama, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hisaya K.","family":"Ono","sequence":"additional","affiliation":[{"name":"Laboratory of Zoonoses, Kitasato University School of Veterinary Medicine, Towada, Aomori, 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