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Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Related Experiment Video

Updated: Jan 12, 2026

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
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Exploring endothelial dysfunction in SLE: cGAS-STING-IRF3 pathway activation by dsDNA.

Zhou Yan1, Li Li2, Zha Shun3

  • 1Department of Nephrology, The First People's Hospital of Yunnan Province /The Affiliated Hospital of Kunming University of Science and Technology, Kunming, China.

Lupus
|November 1, 2025
PubMed
Summary

Extracellular double-stranded DNA (dsDNA) directly damages endothelial cells by activating the cGAS-STING-IRF3 pathway, leading to vascular injury in systemic lupus erythematosus (SLE). Targeting this pathway may offer new SLE treatments.

Keywords:
Systemic lupus erythematosuscGAS-STING-IRF3 pathwaydsDNAvascular endothelial injury

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Area of Science:

  • Immunology
  • Vascular Biology
  • Molecular Medicine

Background:

  • Systemic lupus erythematosus (SLE) is linked to anti-double stranded DNA (anti-dsDNA) antibodies and endothelial dysfunction.
  • The precise mechanisms connecting extracellular DNA to vascular injury in SLE are not fully understood.

Purpose of the Study:

  • To investigate the direct impact of extracellular double-stranded DNA (dsDNA) on endothelial cells.
  • To elucidate the molecular pathways involved in dsDNA-induced endothelial injury.
  • To correlate these findings with endothelial dysfunction markers in SLE patients.

Main Methods:

  • Collected clinical samples from SLE patients and healthy controls.
  • Utilized human umbilical vein endothelial cells (HUVECs) for in vitro studies.
  • Employed cell viability assays, ELISA, RT-qPCR, Western blot, and immunofluorescence to assess endothelial injury and signaling pathways.

Main Results:

  • SLE patients, especially those with anti-dsDNA antibodies, exhibited elevated serum levels of von Willebrand factor (vWF), soluble thrombomodulin (sTM), and E-selectin.
  • In vitro, dsDNA exposure reduced HUVEC viability and upregulated vWF, sTM, and E-selectin secretion.
  • dsDNA activated the cGAS-STING-IRF3 signaling pathway in endothelial cells, confirmed by increased gene and protein expression and enhanced cGAS localization.

Conclusions:

  • Cell-free dsDNA directly induces endothelial dysfunction via the cGAS-STING-IRF3 pathway.
  • This mechanism contributes to vascular injury observed in SLE.
  • The cGAS-STING-IRF3 axis presents a potential therapeutic target for SLE and related conditions.