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Polarization of human gingival fibroblasts by Th1-, Th2-, Th17-, and Treg-derived cytokines

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dc.contributor.authorHa, DY-
dc.contributor.authorJung, JS-
dc.contributor.authorChoi, GH-
dc.contributor.authorJi, S-
dc.date.accessioned2023-03-24T06:27:05Z-
dc.date.available2023-03-24T06:27:05Z-
dc.date.issued2022-
dc.identifier.issn0022-3484-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/25133-
dc.description.abstractBACKGROUND AND OBJECTIVE: The purpose of this study was to evaluate whether gingival fibroblasts (GFs) can be differently activated and polarized into distinct functional subtypes by T-helper (Th) cytokines. METHODS: Gingival fibroblasts were stimulated with interferon (IFN)-gamma, interleukin (IL)-4, IL-17, and transforming growth factor (TGF)-beta, representative cytokines of Th1, Th2, Th17, and regulatory T cells, respectively, and the gene expression profiles were analyzed by microarray. Differentially expressed genes (DEGs) in GFs stimulated by 4 cytokines were screened, and a gene ontology (GO) analysis of the DEGs was conducted. To confirm the reliability of the microarray results, the DEGs that showed the largest differences compared with non-stimulated GFs were further analyzed by RT-PCR. To evaluate the effect of polarization on GFs responses to lipopolysaccharide (LPS), GFs stimulated by 4 cytokines were further stimulated with Escherichia coli LPS and mRNA levels of several genes were analyzed using RT-PCR. RESULTS: Differentially expressed genes by 4 Th cytokines were enriched in different GO terms, and the patterns of gene expression on GFs were shown functionally different. GFs stimulated with IFN-gamma (GF(IFN-gamma)) up-regulated the expression of chemokines (chemokine (C-X-C motif) ligand (CXCL)9, -10, -11, chemokine (C-C motif) ligand (CCL)8), molecules involved in antigen presentation, complement component 3 (C3), and other immune response-related molecules, whereas they down-regulated the expression of several types of collagen, extracellular matrix (ECM) components, and DNA replication and nuclear protein-related molecules. By contrast, GF(IL-4) up-regulated the expression of ECM components, cell adhesion molecules, and tissue development-related molecules and down-regulated the expression of chemokines (CXCL10 and CXCL8) and adaptive immune response-related molecules. GF(IL-17) up-regulated the expression of chemokines and other molecules for neutrophil infiltration and activation, the pro-inflammatory cytokine IL-6, and C3. GF(TGF-beta) up-regulated the expression of cell growth-related molecules, ECM components, several types of collagen, and cell adhesion molecules and down-regulated the expression of molecules related to complement activation and bacterial recognition. GFs stimulated by 4 cytokines responded differently to LPS. CONCLUSION: These results show that Th cytokines can polarize GFs into cells with functionally distinct features: immune-activating but tissue-destructive GF(IFN-gamma), tissue-reparative, and immune-inhibiting GF(IL-4), highly pro-inflammatory GF(IL-17), and potent tissue-reparative GF(TGF-beta).-
dc.language.isoen-
dc.subject.MESHChemokines-
dc.subject.MESHCytokines-
dc.subject.MESHFibroblasts-
dc.subject.MESHHumans-
dc.subject.MESHInterleukin-17-
dc.subject.MESHInterleukin-4-
dc.subject.MESHLigands-
dc.subject.MESHLipopolysaccharides-
dc.subject.MESHReproducibility of Results-
dc.subject.MESHT-Lymphocytes, Regulatory-
dc.subject.MESHTransforming Growth Factor beta-
dc.titlePolarization of human gingival fibroblasts by Th1-, Th2-, Th17-, and Treg-derived cytokines-
dc.typeArticle-
dc.identifier.pmid35212397-
dc.subject.keywordcellular immunology-
dc.subject.keywordcytokines-
dc.subject.keywordfibroblasts-
dc.subject.keywordperiodontal disease-
dc.subject.keywordT-helper cells-
dc.contributor.affiliatedAuthorJung, JS-
dc.contributor.affiliatedAuthorJi, S-
dc.type.localJournal Papers-
dc.identifier.doi10.1111/jre.12978-
dc.citation.titleJournal of periodontal research-
dc.citation.volume57-
dc.citation.number3-
dc.citation.date2022-
dc.citation.startPage487-
dc.citation.endPage501-
dc.identifier.bibliographicCitationJournal of periodontal research, 57(3). : 487-501, 2022-
dc.embargo.liftdate9999-12-31-
dc.embargo.terms9999-12-31-
dc.identifier.eissn1600-0765-
dc.relation.journalidJ000223484-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Dentistry
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