{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T00:15:17Z","timestamp":1787184917333,"version":"build-2736575974"},"reference-count":51,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2019,8,6]],"date-time":"2019-08-06T00:00:00Z","timestamp":1565049600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100007225","name":"Ministry of Science and Technology","doi-asserted-by":"publisher","award":["MOST106\u20102314\u2010B\u2010006\u2010057\u2010MY3"],"award-info":[{"award-number":["MOST106\u20102314\u2010B\u2010006\u2010057\u2010MY3"]}],"id":[{"id":"10.13039\/100007225","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004737","name":"National Health Research Institutes","doi-asserted-by":"publisher","award":["NHRI\u2010106A1\u2010MRCO\u20100517177"],"award-info":[{"award-number":["NHRI\u2010106A1\u2010MRCO\u20100517177"]}],"id":[{"id":"10.13039\/501100004737","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2019,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The role of redox regulation in immune\u2010mediated arthritis has been previously described. However, the relationship between innate immune cells, including innate lymphoid cells (ILCs) and phagocyte\u2010derived ROS, in this process remains unclear. Here, we characterize ILCs and measure the IL\u20101 family cytokines along with other cytokines relevant to ILC functions and development in serum\u2010induced arthritic joints in wild type and phagocytic NADPH oxidase (NOX2)\u2010deficient\n                    <jats:italic>\n                      Ncf1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    mice. We found more severe serum\u2010induced joint inflammation and increased NCR\n                    <jats:sup>+<\/jats:sup>\n                    ILC3s in inflamed joints of\n                    <jats:italic>\n                      Ncf1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    mice. Furthermore, in vitro stimulation with IL\u20101\u03b2 on Tbet\n                    <jats:sup>+<\/jats:sup>\n                    ILC1s from joints facilitated their differentiation into ROR\u2010\u03b3t\n                    <jats:sup>+<\/jats:sup>\n                    ILC3s. Moreover, treatment with IL\u20101 antagonists effectively lowered the proportions of NCR\n                    <jats:sup>+<\/jats:sup>\n                    ILC3s and IL\u201017A producing ILC3s in\n                    <jats:italic>\n                      Ncf1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    arthritic mice and ameliorated the joint inflammation. These results suggest that NOX2 is an essential regulator of ILC transdifferentiation and may mediate this process in a redox\u2010dependent manner through IL\u20101\u03b2 production in the inflammatory joint. Our findings shed important light on the role of ILCs in the initiation and progression in tissue inflammation and delineate a novel innate immune cell\u2010mediated pathogenic mechanism through which redox regulation may determine the direction of immune responses in joints.\n                  <\/jats:p>","DOI":"10.1002\/eji.201948141","type":"journal-article","created":{"date-parts":[[2019,7,27]],"date-time":"2019-07-27T02:34:37Z","timestamp":1564194877000},"page":"2063-2073","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Increased ILC3s associated with higher levels of IL\u20101\u03b2 aggravates inflammatory arthritis in mice lacking phagocytic NADPH oxidase"],"prefix":"10.1002","volume":"49","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8312-5121","authenticated-orcid":false,"given":"Tzu\u2010Yi","family":"Chan","sequence":"first","affiliation":[{"name":"Institute of Clinical Medicine National Cheng\u2010Kung University Medical College  Tainan Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chia\u2010Liang","family":"Yen","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine National Cheng\u2010Kung University Medical College  Tainan Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ya\u2010Fang","family":"Huang","sequence":"additional","affiliation":[{"name":"National Laboratory Animal Center National Applied Research Laboratories  Tainan Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pei\u2010Chi","family":"Lo","sequence":"additional","affiliation":[{"name":"Division of Organ Transplantation Department of Surgery Osaka University. 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