ArticleJCI insight2024
Histone demethylase JARID1C/KDM5C regulates Th17 cells by increasing IL-6 expression in diabetic plasmacytoid dendritic cells.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- The histone demethylase KDM5C aggravates titanium particle-induced osteolysis by promoting macrophage inflammation and osteoclastogenesis.Cellular and molecular life sciences : CMLS · 2026Article
- How to Employ Trained Immunity and Trained Immunity-Based Vaccines to Inhibit Allergic Inflammation.Vaccines · 2026Review
- Clinical value of IL-17-targeted intervention in tissue injury repair: from bidirectional mechanisms to therapeutic strategies.Frontiers in immunology · 2026Review
- Immune imbalance markers: key factors in early recognition of multidrug-resistant bacterial infections in non-immunocompromised VAP patients.Frontiers in immunology · 2026Article
- Mechanisms and Interventions of Diabetic Wound Healing.Current diabetes reviews · 2026Review
- Dual role of IL-17A in COPD: amplifier of inflammatory cascades and mediator of airway remodeling and alveolar destruction.Frontiers in immunology · 2026Review
- IL-17A is increased in diabetic wounds and impairs keratinocyte function via histone demethylase JMJD3.Nature communications · 2025Article
- An endoplasmic reticulum stress-responsive nanocomposite hydrogel for diabetic wound healing through a fibroblast-immune cell dual regulation hub.Journal of nanobiotechnology · 2025Article
- Zn-DHM nanozymes regulate metabolic and immune homeostasis for early diabetic wound therapy.Bioactive materials · 2025Article
- Mechanisms of Impaired Wound Healing in Type 2 Diabetes: The Role of Epigenetic Factors.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- A miRNA cocktail orchestrates coordinated cellular responses to promote diabetic wound healing.Burns & trauma · 2025Article
- Identification of Neutrophil Extracellular Trap-Related Biomarkers in Diabetic Foot Ulcers Based on Bioinformatics.Journal of inflammation research · 2025Article
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Authors and funding
16 authors.
Funding
Abstract
Plasmacytoid dendritic cells (pDCs) are first responders to tissue injury, where they prime naive T cells. The role of pDCs in physiologic wound repair has been examined, but little is known about pDCs in diabetic wound tissue and their interactions with naive CD4+ T cells. Diabetic wounds are characterized by increased levels of inflammatory IL-17A cytokine, partly due to increased Th17 CD4+ cells. This increased IL-17A cytokine, in excess, impairs tissue repair. Here, using human tissue and murine wound healing models, we found that diabetic wound pDCs produced excess IL-6 and TGF-β and that these cytokines skewed naive CD4+ T cells toward a Th17 inflammatory phenotype following cutaneous injury. Further, we identified that increased IL-6 cytokine production by diabetic wound pDCs is regulated by a histone demethylase, Jumonji AT-rich interactive domain 1C histone demethylase (JARID1C). Decreased JARID1C increased IL-6 transcription in diabetic pDCs, and this process was regulated upstream by an IFN-I/TYK2/JAK1,3 signaling pathway. When inhibited in nondiabetic wound pDCs, JARID1C skewed naive CD4+ T cells toward a Th17 phenotype and increased IL-17A production. Together, this suggests that diabetic wound pDCs are epigenetically altered to increase IL-6 expression that then affects T cell phenotype. These findings identify a therapeutically manipulable pathway in diabetic wounds.
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