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Emerging role of bystander T cell activation in autoimmune diseases

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dc.contributor.authorShim, Chae-Hyeon-
dc.contributor.authorCho, Sookyung-
dc.contributor.authorShin, Young-Mi-
dc.contributor.authorChoi, Je-Min-
dc.date.accessioned2022-07-06T10:14:46Z-
dc.date.available2022-07-06T10:14:46Z-
dc.date.created2022-04-06-
dc.date.issued2022-02-
dc.identifier.issn1976-6696-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/139497-
dc.description.abstractAutoimmune disease is known to be caused by unregulated selfantigen-specific T cells, causing tissue damage. Although antigen specificity is an important mechanism of the adaptive immune system, antigen non-related T cells have been found in the inflamed tissues in various conditions. Bystander T cell activation refers to the activation of T cells without antigen recognition. During an immune response to a pathogen, bystander activation of self-reactive T cells via inflammatory mediators such as cytokines can trigger autoimmune diseases. Other antigen-specific T cells can also be bystander-activated to induce innate immune response resulting in autoimmune disease pathogenesis along with self-antigen-specific T cells. In this review, we summarize previous studies investigating bystander activation of various T cell types (NKT, gamma delta T cells, MAIT cells, conventional CD4+, and CD8+ T cells) and discuss the role of innate-like T cell response in autoimmune diseases. In addition, we also review previous findings of bystander T cell function in infection and cancer. A better understanding of bystander-activated T cells versus antigenstimulated T cells provides a novel insight to control autoimmune disease pathogenesis.-
dc.language영어-
dc.language.isoen-
dc.publisherKOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY-
dc.titleEmerging role of bystander T cell activation in autoimmune diseases-
dc.typeArticle-
dc.contributor.affiliatedAuthorChoi, Je-Min-
dc.identifier.doi10.5483/BMBRep.2022.55.2.183-
dc.identifier.scopusid2-s2.0-85125290815-
dc.identifier.wosid000763606900001-
dc.identifier.bibliographicCitationBMB REPORTS, v.55, no.2, pp.57 - 64-
dc.relation.isPartOfBMB REPORTS-
dc.citation.titleBMB REPORTS-
dc.citation.volume55-
dc.citation.number2-
dc.citation.startPage57-
dc.citation.endPage64-
dc.type.rimsART-
dc.type.docTypeReview-
dc.identifier.kciidART002813067-
dc.description.journalClass1-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.subject.keywordPlusIN-VIVO-
dc.subject.keywordPlusMEMORY CD4(+)-
dc.subject.keywordPlusINNATE-LIKE-
dc.subject.keywordPlusIFN-GAMMA-
dc.subject.keywordPlusNKT CELLS-
dc.subject.keywordPlusVIRUS-
dc.subject.keywordPlusSTIMULATION-
dc.subject.keywordPlusLYMPHOCYTES-
dc.subject.keywordPlusIL-1-
dc.subject.keywordPlusPROLIFERATION-
dc.subject.keywordAuthorAntigen specificity-
dc.subject.keywordAuthorAutoimmune disease-
dc.subject.keywordAuthorBystander T cell activation-
dc.subject.keywordAuthorInnate-like functions-
dc.identifier.urlhttps://www.bmbreports.org/journal/view.html?doi=10.5483/BMBRep.2022.55.2.183-
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