{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T07:53:30Z","timestamp":1740124410444,"version":"3.37.3"},"reference-count":44,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2018,6,25]],"date-time":"2018-06-25T00:00:00Z","timestamp":1529884800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["DK092882DK100500"],"award-info":[{"award-number":["DK092882DK100500"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Contact Dermatitis"],"published-print":{"date-parts":[[2018,10]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Genetic background influences allergic immune responses to environmental stimuli. Non\u2010obese diabetic (NOD) mice are highly susceptible to environmental stimuli. Little is known about the interaction of autoimmune genetic factors with innate immunity in allergies, especially skin hypersensitivity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objectives<\/jats:title><jats:p>To study the interplay of innate immunity and autoimmune genetic factors in contact hypersensitivity (CHS) by using various innate immunity\u2010deficient NOD mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Toll\u2010like receptor (TLR) 2\u2010deficient, TLR9\u2010deficient and MyD88\u2010deficient NOD mice were used to investigate CHS. The cellular mechanism was determined by flow cytometry in\u2009vitro and adoptive cell transfer in\u2009vivo. To investigate the role of MyD88 in dendritic cells (DCs) in CHS, we also used CD11c<jats:sup>MyD88+<\/jats:sup>\u2009MyD88<jats:sup>\u2212\/\u2212<\/jats:sup> NOD mice, in which MyD88 is expressed only in CD11c<jats:sup>+<\/jats:sup> cells<jats:bold>.<\/jats:bold><\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We found that innate immunity negatively regulates CHS, as innate immunity\u2010deficient NOD mice developed exacerbated CHS accompanied by increased numbers of skin\u2010migrating CD11c<jats:sup>+<\/jats:sup> DCs expressing higher levels of major histocompatibility complex II and CD80. Moreover, MyD88<jats:sup>\u2212\/\u2212<\/jats:sup> NOD mice had increased numbers of CD11c<jats:sup>+<\/jats:sup>\u2009CD207<jats:sup>\u2212<\/jats:sup>\u2009CD103<jats:sup>+<\/jats:sup> DCs and activated T effector cells in the skin\u2010draining lymph nodes. Strikingly, re\u2010expression of MyD88 in CD11c<jats:sup>+<\/jats:sup> DCs (CD11c<jats:sup>MyD88+<\/jats:sup>\u2009MyD88<jats:sup>\u2212\/\u2212<\/jats:sup> NOD mice) restored hyper\u2010CHS to a normal level in MyD88<jats:sup>\u2212\/\u2212<\/jats:sup> NOD mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our results suggest that the autoimmune\u2010prone NOD genetic background aggravates CHS regulated by innate immunity, through DCs and T effector cells.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cod.13046","type":"journal-article","created":{"date-parts":[[2018,6,26]],"date-time":"2018-06-26T04:34:25Z","timestamp":1529987665000},"page":"197-207","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Regulation of contact sensitivity in non\u2010obese diabetic (NOD) mice by innate immunity"],"prefix":"10.1111","volume":"79","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0388-2382","authenticated-orcid":false,"given":"Marian","family":"Szczepanik","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Section of Endocrinology Yale University School of Medicine  New Haven Connecticut"},{"name":"Department of Medical Biology, Health Science Faculty Jagiellonian University Medical College  Krakow Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Monika","family":"Majewska\u2010Szczepanik","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Section of Endocrinology Yale University School of Medicine  New Haven Connecticut"},{"name":"Department of Medical Biology, Health Science Faculty Jagiellonian University Medical College  Krakow Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Florence S.","family":"Wong","sequence":"additional","affiliation":[{"name":"Division of Infection and Immunity Cardiff University School of Medicine  Cardiff UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paulina","family":"Kowalczyk","sequence":"additional","affiliation":[{"name":"Department of Medical Biology, Health Science Faculty Jagiellonian University Medical College  Krakow Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chandrashekhar","family":"Pasare","sequence":"additional","affiliation":[{"name":"Department of Immunology University of Texas Southwestern Medical Center  Dallas Texas"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8805-2934","authenticated-orcid":false,"given":"Li","family":"Wen","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Section of Endocrinology Yale University School of Medicine  New Haven 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