ArticleInvestigative ophthalmology & visual science2025
S100A8/A9 Promotes Dendritic Cell-Mediated Th17 Cell Response in Sjögren's Dry Eye Disease by Regulating the Acod1/STAT3 Pathway.
Article in Investigative ophthalmology & visual science, 2025. 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 Role of S100A8/A9 in Autoimmune Eye Diseases: From Pathogenesis to Targeted Therapy.Investigative ophthalmology & visual science · 2026Review
- Review
- S100A9 deletion ameliorates acute lung injury by attenuating excessive neutrophil activation via activating the NRF2/HO-1 signaling axis.Respiratory research · 2026Article
- Antioxidant Peptides fromMarine drugs · 2026Article
- Sfrp2 in Microglia Inhibited S100a8-Mediated Neuroinflammation and Protected Neural Damage Following Retinal Ischemia-Reperfusion.Investigative ophthalmology & visual science · 2026Article
- Research progress in animal models of dry eye disease: Types, mechanisms, and application prospects.Animal models and experimental medicine · 2026Review
- Serum S100A8 as a potential biomarker for diagnosis of antiphospholipid syndrome and risk stratification among aPL carriers.Lupus science & medicine · 2026Article
- The S100A8/A9-NETosis feedback loop in sepsis: potential mechanisms, immune crosstalk, and therapeutic targeting.Frontiers in immunology · 2026Review
- Mechanisms of Mesenchymal Stem Cell-Derived Exosomes in Dry Eye Disease: From Inflammation Pathways to Therapeutic Prospects.Stem cells international · 2026Review
- Tlr9 expression protects against Tlr7-dependent exocrine gland and systemic disease manifestations in primary Sjögren's disease in a sex-biased manner.Journal of autoimmunity · 2025Article
- Single-Cell RNA Sequencing Revealed Functional Conjunctival Keratinocytes Loss via TGF-β-Wnt/β-Catenin Signaling in Sjögren's Syndrome Related Dry Eye.Investigative ophthalmology & visual science · 2025Article
- Expression and clinical significance of S100A8/9 in adults with secondary phagocytic lymphohistiocytosis.Frontiers in molecular biosciences · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: To investigate the role of S100A8/A9 in the pathogenesis of Sjögren's dry eye disease (SjDED) and explore its potential mechanism of action. Methods: S100A8/A9 expression was determined by western blot and quantitative real-time polymerase chain reaction (qRT-PCR). Tear secretion, corneal fluorescein staining, and hematoxylin and eosin staining were used to evaluate the effect of paquinimod, a S100A8/A9 inhibitor, on dry eye disease in nonobese diabetic (NOD) mice. Immune cell infiltration and percentage were assessed by immunofluorescence and flow cytometry. Proinflammatory cytokine levels were examined by qRT-PCR or ELISA. The mechanism of action was analyzed using western blot, immunofluorescence, and chromatin immunoprecipitation. Results: S100A8/A9 was upregulated in peripheral blood mononuclear cells of patients with SjDED and lacrimal glands (LGs) of SjDED mice. The upregulation of S100A8/A9 was correlated with the dry eye severity and inflammatory infiltration levels in LGs. Administration of paquinimod ameliorated clinical and histopathological phenotypes of SjDED mice and reduced the proportion of Th17 cells in LGs, lymph nodes, and spleens. Further experiments revealed that S100A8/A9 did not directly affect Th17 generation and function but upregulated the expression of major histocompatibility complex Ⅱ (MHC Ⅱ) and Th17-polarizing cytokines in dendritic cells (DCs) to augment Th17 cell response. Mechanistically, S100A8/A9 induced the expression of Acod1 and thereby promoted the activation and nuclear translocation of signal transducer and activator of transcription 3 (STAT3), resulting in increased Il23a transcription. STAT3 activator reversed the therapeutic effect of paquinimod on SjDED mice. Conclusions: S100A8/A9 activated the Acod1/STAT3 pathway to promote DC-driven Th17 cell responses in SjDED. The S100A8/A9/Acod1/STAT3 pathway may represent a promising therapeutic target for SjDED.
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