ArticleMediators of inflammation2014
Clinical significance of IL-23 regulating IL-17A and/or IL-17F positive Th17 cells in chronic periodontitis.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- A Systematic Review and Meta-Analysis on Multiple Cytokine Gene Polymorphisms in the Pathogenesis of Periodontitis.Frontiers in immunology · 2021Pooled it
- Impact of anti-TNF and anti-IL-12/IL-23 antibody therapy on periodontal inflammation and gingival crevicular fluid IL-6 in patients with inflammatory bowel diseases.Frontiers in immunology · 2026Article
- Cytokines in gingivitis and periodontitis: from pathogenesis to therapeutic targets.Frontiers in immunology · 2024Review
- High-Glucose Media Reduced the Viability and Induced Differential Pro-Inflammatory Cytokines in Human Periodontal Ligament Fibroblasts.Biomolecules · 2023Article
- The Composition of Subgingival Microbiome in Hidradenitis Suppurativa and Periodontitis Patients.Pathogens (Basel, Switzerland) · 2023Article
- The Prevalence of Periodontitis and Assessment of Oral Micro-Biota in Patients with Hidradenitis Suppurativa: A Descriptive Cross-Sectional Study.Journal of clinical medicine · 2022Article
- Periodontal Conditions and Whole Salivary IL-17A and -23 Levels among Young AdultInternational journal of environmental research and public health · 2020Article
- Chronic atrophic gastritis aggravate chronic periodontitis with Helicobacter pylori infection and CD4+Th cytokines infiltration.Histology and histopathology · 2020Article
- Plasma IL-23 and IL-5 as surrogate markers of lesion metabolic activity in patients with hepatic alveolar echinococcosis.Scientific reports · 2018Article
- The imbalance of Th17/Treg cells is involved in the progression of nonalcoholic fatty liver disease in mice.BMC immunology · 2017Article
- Article
- Interleukin-17 inhibitors. A new era in treatment of psoriasis and other skin diseases.Postepy dermatologii i alergologii · 2016Review
- Interleukin-17A Gene Variability in Patients with Type 1 Diabetes Mellitus and Chronic Periodontitis: Its Correlation with IL-17 Levels and the Occurrence of Periodontopathic Bacteria.Mediators of inflammation · 2016Article
- Role of Porphyromonas gingivalis HmuY in Immunopathogenesis of Chronic Periodontitis.Mediators of inflammation · 2016Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the expression level and clinical significance of (IL-17A(+) and/or IL-17F(+)) Th17 cells under IL-23 regulation in patients of chronic periodontitis (CP) and healthy controls (HC). MATERIALS AND
methodsThe whole peripheral blood samples were collected from 30 CP patients and 25 healthy controls. Flow cytometry was used to test the (IL-17A(+) and/or IL-17F(+)) Th17 expression level. Recombinant human IL-23 (rhIL-23) was used to detect Th17 differentiation and expansion. Correlation coefficient analysis between Th17 expression level and clinical parameters was analyzed by SPSS software.
resultsFlow cytometry results showed that IL-17A(+)IL-17F(-) and IL-17A(-)IL-17F(+) Th17 were both increased in CP group than in HC group (P < 0.01), while, under recombinant human IL-23 (rhIL-23) stimulation, the number of IL-17A(+)IL-17F(-) Th17 cells was significantly increased in both CP and HC groups (P < 0.01). Interestingly, IL-17A(-)IL-17F(+) Th17 cells were only increased in CP group after rhIL-23 stimulation. Additionally, correlation coefficient analysis showed significant correlation between IL-17A(+)IL-17F(-) Th17 cell and attachment loss or probing depth (P < 0.05).
conclusionsThis study indicates that both the IL-17A(+)IL-17F(-) and IL-17A(-)IL-17F(+) Th17 cells may be involved in pathogenesis of periodontitis. The role of these Th17 cells in the disease pathogenesis needs to be further investigated.
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