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Alleviating psoriatic skin inflammation through augmentation of Treg cells via CTLA-4 signaling peptide

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dc.contributor.authorLee, Woo-Sung-
dc.contributor.authorNam, Kyung-Ho-
dc.contributor.authorKim, Jong Hoon-
dc.contributor.authorKim, Won-Ju-
dc.contributor.authorKim, Jeong Eun-
dc.contributor.authorEui-Cheol Shin-
dc.contributor.authorKim, Gil-Ran-
dc.contributor.authorChoi, Je-Min-
dc.date.accessioned2023-11-03T22:00:11Z-
dc.date.available2023-11-03T22:00:11Z-
dc.date.created2023-10-23-
dc.date.issued2023-09-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/14083-
dc.description.abstractPsoriasis is a chronic inflammatory skin disease characterized by hyperplasia of keratinocytes and immune cell infiltration. The IL-17-producing T cells play a key role in psoriasis pathogenesis, while regulatory T (Treg) cells are diminished during psoriatic inflammation. Current psoriasis treatments largely focus on IL-17 and IL-23, however, few studies have explored therapeutic drugs targeting an increase of Treg cells to control immune homeostasis. In this study, we investigated the effects of a cytotoxic T lymphocyte antigen-4 (CTLA-4) signaling peptide (dNP2-ctCTLA-4) in Th17, Tc17, gamma delta T cells, Treg cells in vitro and a mouse model of psoriasis. Treatment with dNP2-ctCTLA-4 peptide showed a significant reduction of psoriatic skin inflammation with increased Treg cell proportion and reduced IL-17 production by T cells, indicating a potential role in modulating psoriatic skin disease. We compared dNP2-ctCTLA-4 with CTLA-4-Ig and found that only dNP2-ctCTLA-4 ameliorated the psoriasis progression, with increased Treg cells and inhibited IL-17 production from gamma delta T cells. In vitro experiments using a T cell-antigen presenting cell co-culture system demonstrated the distinct mechanisms of dNP2-ctCTLA-4 compared to CTLA-4-Ig in the induction of Treg cells. These findings highlight the therapeutic potential of dNP2-ctCTLA-4 peptide in psoriasis by augmenting Treg/Teff ratio, offering a new approach to modulating the disease.-
dc.language영어-
dc.publisherFrontiers Media S.A.-
dc.titleAlleviating psoriatic skin inflammation through augmentation of Treg cells via CTLA-4 signaling peptide-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid001077572100001-
dc.identifier.scopusid2-s2.0-85173627173-
dc.identifier.rimsid81966-
dc.contributor.affiliatedAuthorEui-Cheol Shin-
dc.identifier.doi10.3389/fimmu.2023.1233514-
dc.identifier.bibliographicCitationFrontiers in Immunology, v.14-
dc.relation.isPartOfFrontiers in Immunology-
dc.citation.titleFrontiers in Immunology-
dc.citation.volume14-
dc.description.journalClass1-
dc.description.journalClass1-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.subject.keywordPlusMAINTENANCE-
dc.subject.keywordPlusIMMUNOLOGY-
dc.subject.keywordPlusRESPONSES-
dc.subject.keywordPlusDELIVERY-
dc.subject.keywordPlusREGULATORY T-CELLS-
dc.subject.keywordPlusCYTOPLASMIC DOMAIN-
dc.subject.keywordPlusATOPIC-DERMATITIS-
dc.subject.keywordPlusGAMMA-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusTRANSDUCTION-
dc.subject.keywordAuthorpsoriasis-
dc.subject.keywordAuthordNP2-ctCTLA-4-
dc.subject.keywordAuthorCTLA-4-Ig-
dc.subject.keywordAuthorTreg cells-
dc.subject.keywordAuthorIL-17A-
Appears in Collections:
Korea Virus Research Institute(한국바이러스기초연구소) > Center for Viral Immunology(바이러스 면역 연구센터) > 1. Journal Papers (저널논문)
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