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IL-25 enhances HSV-1 replication by inhibiting filaggrin expression, and acts synergistically with Th2 cytokines to enhance HSV-1 replication.

DC Field Value Language
dc.contributor.authorKim, BE-
dc.contributor.authorBin, L-
dc.contributor.authorYe, YM-
dc.contributor.authorRamamoorthy, P-
dc.contributor.authorLeung, DY-
dc.date.accessioned2014-05-22T05:48:13Z-
dc.date.available2014-05-22T05:48:13Z-
dc.date.issued2013-
dc.identifier.issn0022-202X-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/10076-
dc.description.abstractAtopic dermatitis (AD) is characterized by epidermal barrier defects and recurrent microbial skin infections. AD patients with a history of eczema herpeticum (ADEH+) have more severe skin disease and more highly T helper type 2 (Th2)-polarized immune responses as compared with uncomplicated AD (ADEH-). However, the mechanisms linking epidermal barrier defects and viral skin infection are not well understood. Recently, it has been reported that interleukin-25 may play a role in augmenting Th2 responses. We examined protein expression of IL-25 in the skin biopsies from normal subjects (n=10), ADEH- (n=18), ADEH+ (n=7), and psoriasis (n=9). IL-25 expression was increased in the skin from ADEH-, ADEH+, and psoriasis as compared with normal skin, and was significantly greater in lesional ADEH+ skin than in lesional ADEH- skin. Importantly, we demonstrated that IL-25 enhances herpes simplex virus (HSV)-1 and vaccinia virus replication by inhibiting filaggrin expression, and IL-25 acts synergistically with IL-4 and IL-13 to enhance HSV-1 replication in vitro. In contrast, IFN-γ inhibited HSV-1 replication in vitro. In addition, we demonstrate that filaggrin is a critical protein to inhibit HSV-1 replication because filaggrin small interfering RNA knockdown enhances HSV-1 replication in vitro. Filaggrin breakdown products, however, inhibited HSV-1 replication in vitro.-
dc.language.isoen-
dc.subject.MESHBiopsy-
dc.subject.MESHGene Expression Regulation-
dc.subject.MESHGene Silencing-
dc.subject.MESHGenotype-
dc.subject.MESHHerpesvirus 1, Human/*physiology-
dc.subject.MESHHumans-
dc.subject.MESHInterferon-gamma/metabolism-
dc.subject.MESHInterleukin-13/metabolism-
dc.subject.MESHInterleukin-17/*physiology-
dc.subject.MESHInterleukin-4/metabolism-
dc.subject.MESHIntermediate Filament Proteins/*metabolism-
dc.subject.MESHKaposi Varicelliform Eruption/complications/*metabolism/virology-
dc.subject.MESHPsoriasis/metabolism-
dc.subject.MESHRNA, Small Interfering/metabolism-
dc.subject.MESHSkin/metabolism-
dc.subject.MESHSkin Diseases/virology-
dc.subject.MESHTh2 Cells/*metabolism-
dc.subject.MESHVaccinia virus/metabolism-
dc.subject.MESHVirus Diseases/metabolism-
dc.subject.MESH*Virus Replication-
dc.titleIL-25 enhances HSV-1 replication by inhibiting filaggrin expression, and acts synergistically with Th2 cytokines to enhance HSV-1 replication.-
dc.typeArticle-
dc.identifier.pmid23657503-
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3785566/-
dc.contributor.affiliatedAuthor예, 영민-
dc.type.localJournal Papers-
dc.identifier.doi10.1038/jid.2013.223-
dc.citation.titleThe Journal of investigative dermatology-
dc.citation.volume133-
dc.citation.number12-
dc.citation.date2013-
dc.citation.startPage2678-
dc.citation.endPage2685-
dc.identifier.bibliographicCitationThe Journal of investigative dermatology, 133(12):2678-2685, 2013-
dc.identifier.eissn1523-1747-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Allergy
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