ArticleInflammation2023
CXCL9, 10, 11/CXCR3 Axis Contributes to the Progress of Primary Sjogren's Syndrome by Activating GRK2 to Promote T Lymphocyte Migration.
Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 18 citations in OpenAlex.
- JAK inhibitor tofacitinib alleviates secretory dysfunction and Th17/Treg imbalance in a Sjögren's disease murine model.Annals of medicine · 2026Article
- Multifaceted roles of chemokines in gastric cancer: From tumor microenvironment modulation to therapeutic targeting (Review).Oncology letters · 2026Review
- Th2 bias and T-cell exhaustion characterize the immunopathology of non-tuberculous mycobacterial pulmonary disease.NPJ systems biology and applications · 2026Article
- CXC Chemokine-Driven Vascular Reprogramming: Modulating Tumor Vasculature to Boost Therapeutic Response.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Deciphering the molecular landscape of Sjögren's disease, mucosa-associated lymphoid tissue lymphoma, and thyroid cancer: unraveling the complexities of disease mechanisms and diagnostic biomarkers.Clinical rheumatology · 2026Article
- Regulation of G protein-coupled receptor kinase 2 and its role in tumors.Journal of translational medicine · 2026Review
- Development of an improved preclinical humanized mouse platform representing the diverse clinical phenotypes of Sjögren's syndrome.Frontiers in immunology · 2026Article
- Deciphering the interferon gene signature spectrum: association with the clinical heterogeneity of Sjögren's disease.Frontiers in immunology · 2026Article
- Fibrosis in Immune-Mediated and Autoimmune Disorders.Journal of clinical medicine · 2025Review
- Exosomes as immunomodulators in autoimmune inflammation: implications for primary Sjögren's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Inhibiting miR-155-5p promotes proliferation of human submandibular gland epithelial cells in primary Sjogren's syndrome by negatively regulating the PI3K/AKT signaling pathwayNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- CRISPR-Cas9 editing ofFrontiers in genome editing · 2025Article
- CD226Frontiers in immunology · 2025Article
- Single-cell transcriptomic analysis uncovers heterogeneity in the labial gland microenvironment of primary Sjögren's syndrome.Journal of translational autoimmunity · 2024Article
- G protein-coupled receptor kinase 2 as a novel therapeutic target for gland fibrosis of Sjögren's syndrome.Acta pharmacologica Sinica · 2024Article
- CXCL9 may serve as a potential biomarker for primary Sjögren's syndrome with extra-glandular manifestations.Arthritis research & therapy · 2024Article
- Immune and non-immune mediators in the fibrosis pathogenesis of salivary gland in Sjögren's syndrome.Frontiers in immunology · 2024Review
- Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Primary Sjogren's syndrome (pSS) is a systemic autoimmune disease that causes dysfunction of secretory glands and the specific pathogenesis is still unknown. The CXCL9, 10, 11/CXCR3 axis and G protein-coupled receptor kinase 2 (GRK2) involved in many inflammation and immunity processes. We used NOD/Ltj mice, a spontaneous SS animal model, to elucidate the pathological mechanism of CXCL9, 10, 11/CXCR3 axis promoting T lymphocyte migration by activating GRK2 in pSS. We found that CD4 + GRK2, Th17 + CXCR3 was apparently increased and Treg + CXCR3 was significantly decreased in the spleen of 4W NOD mice without sicca symptom compared to ICR mice (control group). The protein levels of IFN-γ, CXCL9, 10, 11 increased in submandibular gland (SG) tissue accompanied by obvious lymphocytic infiltration and Th17 cells overwhelmingly infiltrated relative to Treg cells at the sicca symptom occurs, and we found that the proportion of Th17 cells was increased, whereas that of Treg cells was decreased in spleen. In vitro, we used IFN-γ to stimulate human salivary gland epithelial cells (HSGECs) co-cultured with Jurkat cells, and the results showed that CXCL9, 10, 11 was increased by IFN-γ activating JAK2/STAT1 signal pathway and Jurkat cell migration increased with the raised of cell membrane GRK2 expression. HSGECs with tofacitinib or Jurkat cells with GRK2 siRNA can reduce the migration of Jurkat cells. The results indicate that CXCL9, 10, 11 significantly increased in SG tissue through IFN-γ stimulating HSGECs, and the CXCL9, 10, 11/CXCR3 axis contributes to the progress of pSS by activating GRK2 to promote T lymphocyte migration.
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Registered trials
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