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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\u2010stimulated GFs were further analyzed by RT\u2010PCR. To evaluate the effect of polarization on GFs responses to lipopolysaccharide (LPS), GFs stimulated by 4 cytokines were further stimulated with <jats:italic>Escherichia coli<\/jats:italic> LPS and mRNA levels of several genes were analyzed using RT\u2010PCR.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Differentially expressed genes by 4\u00a0Th cytokines were enriched in different GO terms, and the patterns of gene expression on GFs were shown functionally different. GFs stimulated with IFN\u2010\u03b3 (GF(IFN\u2010\u03b3)) up\u2010regulated the expression of chemokines (chemokine (C\u2010X\u2010C motif) ligand (CXCL)9, \u221210, \u221211, chemokine (C\u2010C motif) ligand (CCL)8), molecules involved in antigen presentation, complement component 3 (C3), and other immune response\u2013related molecules, whereas they down\u2010regulated the expression of several types of collagen, extracellular matrix (ECM) components, and DNA replication and nuclear protein\u2013related molecules. By contrast, GF(IL\u20104) up\u2010regulated the expression of ECM components, cell adhesion molecules, and tissue development\u2013related molecules and down\u2010regulated the expression of chemokines (CXCL10 and CXCL8) and adaptive immune response\u2013related molecules. GF(IL\u201017) up\u2010regulated the expression of chemokines and other molecules for neutrophil infiltration and activation, the pro\u2010inflammatory cytokine IL\u20106, and C3. GF(TGF\u2010\u03b2) up\u2010regulated the expression of cell growth\u2013related molecules, ECM components, several types of collagen, and cell adhesion molecules and down\u2010regulated the expression of molecules related to complement activation and bacterial recognition. GFs stimulated by 4 cytokines responded differently to LPS.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These results show that Th cytokines can polarize GFs into cells with functionally distinct features: immune\u2010activating but tissue\u2010destructive GF(IFN\u2010\u03b3), tissue\u2010reparative, and immune\u2010inhibiting GF(IL\u20104), highly pro\u2010inflammatory GF(IL\u201017), and potent tissue\u2010reparative GF(TGF\u2010\u03b2).<\/jats:p><\/jats:sec>","DOI":"10.1111\/jre.12978","type":"journal-article","created":{"date-parts":[[2022,2,25]],"date-time":"2022-02-25T10:20:10Z","timestamp":1645784410000},"page":"487-501","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Polarization of human gingival fibroblasts by Th1\u2010, Th2\u2010, Th17\u2010, and Treg\u2010derived cytokines"],"prefix":"10.1111","volume":"57","author":[{"given":"Da Young","family":"Ha","sequence":"first","affiliation":[{"name":"Department of Periodontology Institute of Oral Health Science Ajou University School of Medicine  Suwon Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jae\u2010Suk","family":"Jung","sequence":"additional","affiliation":[{"name":"Department of Periodontology Institute of Oral Health Science Ajou University School of Medicine  Suwon Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Geum Hee","family":"Choi","sequence":"additional","affiliation":[{"name":"Department of Periodontology Institute of Oral Health Science Ajou University School of Medicine  Suwon Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9720-6731","authenticated-orcid":false,"given":"Suk","family":"Ji","sequence":"additional","affiliation":[{"name":"Department of Periodontology Institute of Oral Health Science Ajou University School of Medicine  Suwon Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2022,2,25]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0765.1993.tb02108.x"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/jre.12248"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1902\/jop.2008.080183"},{"key":"e_1_2_7_5_1","first-page":"235","article-title":"Pathogenesis of inflammatory periodontal disease. 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