Publication:
Mesenchymal stem cells derived from human dental follicle modulate the aberrant immune response in atopic dermatitis

dc.contributor.coauthorGenç, Deniz
dc.contributor.coauthorÖzgen, Züleyha
dc.contributor.coauthorDuran, Yazgül
dc.contributor.coauthorGöker, Kamil
dc.contributor.coauthorBarış, Safa
dc.contributor.coauthorErgun, Tülin
dc.contributor.coauthorAkkoç, Tunç
dc.contributor.departmentN/A
dc.contributor.kuauthorZibandeh, Noushin
dc.contributor.kuprofileResearcher
dc.contributor.researchcenterKoç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM)
dc.contributor.schoolcollegeinstituteN/A
dc.contributor.yokidN/A
dc.date.accessioned2024-11-10T00:07:18Z
dc.date.issued2021
dc.description.abstractBackground: Atopic dermatitis (AD) is an inflammatory cutaneous disorder. The advancements in the understanding of AD immunological pathogenesis have caused the development of therapies that suppress the dysregulated immune response. We aimed to evaluate the immunomodulatory effect of dental stem cells (dental follicle-mesenchymal stem cells [DF-MSCs]) on AD patients. Materials & methods: We investigated the immunoregulatory potential of DF-MSCs on T cell response in AD and compared them with psoriasis and healthy individuals and the underlying mechanisms. Results: DF-MSCs significantly reduced Fas, FasL and TNFR II frequency in T cells, increased naive T cell population while reducing memory T cell, decreased inflammatory cytokine levels and promoted Tregs frequency in the AD population. Conclusion: These results imply that DF-MSCs are modulating inflammation through decreasing T cell apoptosis, inducing Treg expansion and stabilizing cytokine levels. Lay abstract Background: Atopic dermatitis (AD) is an inflammatory cutaneous disorder characterized by immune-mediated inflammation and epidermal barrier dysfunction. There is no definite solution for the treatment of AD. We aimed to evaluate the immunomodulatory and immunosuppressive effect of dental stem cells (dental follicle-mesenchymal stem cell [DF-MSCs]) on AD. Materials & methods: We investigated the immunoregulatory potential of DF-MSCs on inflammatory response in AD and compared them with psoriasis and healthy individuals and the mechanism underlying it. Results: DF-MSCs significantly reduced apoptosis-related markers in immune cells, decreased inflammatory cytokine levels and promoted Treg frequency in the AD. Conclusion: Our findings provide basic evidence for the potential role of DF-MSCs as a cellular therapy option in the treatment of AD and shed light on future clinical studies.
dc.description.indexedbyWoS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.issue10
dc.description.openaccessNO
dc.description.publisherscopeInternational
dc.description.sponsorshipMarmara University Scientific Research Committee (BAPKO) [SAG-C-DRP-200716-0373] This project was supported by Marmara University Scientific Research Committee (BAPKO) Project No: SAG-C-DRP-200716-0373. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
dc.description.volume13
dc.identifier.doi10.2217/imt-2020-0257
dc.identifier.eissn1750-7448
dc.identifier.issn1750-743X
dc.identifier.quartileQ4
dc.identifier.scopus2-s2.0-85107586298
dc.identifier.urihttp://dx.doi.org/10.2217/imt-2020-0257
dc.identifier.urihttps://hdl.handle.net/20.500.14288/16763
dc.identifier.wos647582400001
dc.keywordsAtopic dermititis
dc.keywordsDental follicle mesenchymal stem cells
dc.keywordsImmunomodulation
dc.keywordsImmunotherapy
dc.keywordsPsoriasis
dc.keywordsRegenarative medicine
dc.languageEnglish
dc.publisherFuture Medicine
dc.sourceImmunotherapy
dc.subjectImmunology
dc.titleMesenchymal stem cells derived from human dental follicle modulate the aberrant immune response in atopic dermatitis
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.authorid0000-0002-4078-8029
local.contributor.kuauthorZibandeh, Noushin

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