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Staged development of long-lived T-cell receptor αβ TH17 resident memory T-cell population to Candida albicans after skin infection

DC Field Value Language
dc.contributor.author박창욱-
dc.contributor.author박창욱-
dc.date.accessioned2018-07-20T12:00:22Z-
dc.date.available2018-07-20T12:00:22Z-
dc.date.issued2018-
dc.identifier.issn0091-6749-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/161627-
dc.description.abstractBACKGROUND: Candida albicans is a dimorphic fungus to which human subjects are exposed early in life, and by adulthood, it is part of the mycobiome of skin and other tissues. Neonatal skin lacks resident memory T (TRM) cells, but in adults the C albicans skin test is a surrogate for immunocompetence. Young adult mice raised under specific pathogen-free conditions are naive to C albicans and have been shown recently to have an immune system resembling that of neonatal human subjects. OBJECTIVE: We studied the evolution of the adaptive cutaneous immune response to Candida species. METHODS: We examined both human skin T cells and the de novo and memory immune responses in a mouse model of C albicans skin infection. RESULTS: In mice the initial IL-17-producing cells after C albicans infection were dermal γδ T cells, but by day 7, αβ TH17 effector T cells were predominant. By day 30, the majority of C albicans-reactive IL-17-producing T cells were CD4 TRM cells. Intravital microscopy showed that CD4 effector T cells were recruited to the site of primary infection and were highly motile 10 days after infection. Between 30 and 90 days after infection, these CD4 T cells became increasingly sessile, acquired expression of CD69 and CD103, and localized to the papillary dermis. These established TRM cells produced IL-17 on challenge, whereas motile migratory memory T cells did not. TRM cells rapidly clear an infectious challenge with C albicans more effectively than recirculating T cells, although both populations participate. We found that in normal human skin IL-17-producing CD4+ TRM cells that responded to C albicans in an MHC class II-restricted fashion could be identified readily. CONCLUSIONS: These studies demonstrate that C albicans infection of skin preferentially generates CD4+ IL-17-producing TRM cells, which mediate durable protective immunity.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherSt Louis, Mosby-
dc.relation.isPartOfJOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleStaged development of long-lived T-cell receptor αβ TH17 resident memory T-cell population to Candida albicans after skin infection-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Dermatology-
dc.contributor.googleauthorChang Ook Park-
dc.contributor.googleauthorXiujun Fu-
dc.contributor.googleauthorXiaodong Jiang-
dc.contributor.googleauthorYoudong Pan-
dc.contributor.googleauthorJessica E. Teague-
dc.contributor.googleauthorNicholas Collins-
dc.contributor.googleauthorTian Tian-
dc.contributor.googleauthorJohn T. O'Malley-
dc.contributor.googleauthorRyan O. Emerson-
dc.contributor.googleauthorJi Hye Kim-
dc.contributor.googleauthorYookyung Jung-
dc.contributor.googleauthorRei Watanabe-
dc.contributor.googleauthorRobert C. Fuhlbrigge-
dc.contributor.googleauthorFrancis R. Carbone-
dc.contributor.googleauthorThomas Gebhardt-
dc.contributor.googleauthorRachael A. Clark-
dc.contributor.googleauthorCharles P. Lin-
dc.contributor.googleauthorThomas S. Kupper-
dc.identifier.doi10.1016/j.jaci.2017.09.042-
dc.contributor.localIdA01716-
dc.contributor.localIdA01716-
dc.contributor.localIdA01716-
dc.relation.journalcodeJ01228-
dc.identifier.eissn1097-6825-
dc.identifier.pmid29128674-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0091674917317372-
dc.subject.keywordCD4(+) T(RM)-
dc.subject.keywordCandida albicans-
dc.subject.keywordIL-17-
dc.subject.keywordResident memory T cells-
dc.subject.keywordT(H)17-
dc.subject.keywordT(RM)-
dc.contributor.alternativeNamePark, Chang Ook-
dc.contributor.affiliatedAuthorPark, Chang Ook-
dc.contributor.affiliatedAuthor박창욱-
dc.contributor.affiliatedAuthor박창욱-
dc.citation.volume142-
dc.citation.number2-
dc.citation.startPage647-
dc.citation.endPage662-
dc.identifier.bibliographicCitationJOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol.142(2) : 647-662, 2018-
dc.identifier.rimsid61650-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers

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