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The STING/type I interferon axis drives the interplay between marginal zone B cells and T follicular helper cells in Sjögren’s disease

Cellular & Molecular Immunology (2025)Cite this article

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Abstract

Type I interferon (IFN-I) is highly prevalent in autoimmune disorders and is intricately involved in disease pathogenesis, including Sjögren’s disease (SjD), also known as Sjögren’s syndrome. Although the T follicular helper (Tfh) cell response has been shown to drive SjD development in a mouse model of experimental Sjögren’s syndrome (ESS), the connection between IFN-I and the Tfh cell response remains unclear. As the activation of stimulator of interferon genes (STING) induces IFN-I production, we first demonstrated that mice deficient in STING or IFN-I signaling presented diminished Tfh cells and were completely resistant to ESS development. However, the STING–IFN-I axis does not directly influence Tfh cell differentiation. Instead, IFN-I signaling in B cells was essential for mounting Tfh cell responses, as evidenced in Cd19CreIfnar1flox mice, which also showed resistance to ESS development. Mechanistic analyses revealed that IFN-I drove CXCR5 expression in innate-like marginal zone B cells via the MEKK3–OCT2 axis, facilitating their migration into the follicular area. Additionally, IFN-I promoted interleukin-6 production in B cells via the MEKK3–ERK5 axis, resulting in hyperactive Tfh cell responses. In SjD patients, STING activation was predominantly observed in circulating CD14+ monocytes and was positively correlated with disease activity and effector T-cell responses. Pharmaceutical inhibition of either STING or IFNAR1 yielded moderate improvements in ESS mice with chronic inflammation, but combination therapy markedly improved outcomes and led to signs of disease remission. Our findings elucidate a novel mechanism by which IFN-I bridges innate and Tfh cell responses, suggesting new therapeutic avenues for SjD and related autoimmune disorders.

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Acknowledgements

This work was supported by the General Research Fund, Hong Kong Research Grants Council (17109123, 17116521 and 27111820), the Mainland-Hong Kong Joint Funding Scheme (MHP/104/22) and the Health and Medical Research Fund (20212601 and 19201121). We are thankful for the technical support from the Center for PanorOmic Sciences (CPOS), University of Hong Kong. Professional English language editing support was provided by AsiaEdit.

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  1. School of Chinese Medicine, the University of Hong Kong, Hong Kong SAR, China

    Yacun Chen, Sulan Yu, Haozhen Yan, Jing Xie & Xiang Lin

  2. Division of Rheumatology and Clinical Immunology, Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR, China

    Philip Hei Li & Iris Yanki Tang

  3. Department of Pathology, Shenzhen University General Hospital, Shenzhen, China

    Hongyun Cheng

  4. State Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong Kong SAR, China

    Xiang Lin

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YC: Validation, Software, Investigation, Formal analysis, Writing—original draft. SY: Investigation. PHL: Resources. JX: Formal analysis, Visualization. IYT: Resources. HC: Investigation. HY: Investigation. XL: Writing—original draft, Writing—review & editing, Visualization, Supervision, Software, Project administration, Methodology, Investigation, Funding acquisition, Conceptualization.

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Chen, Y., Yu, S., Li, P.H. et al. The STING/type I interferon axis drives the interplay between marginal zone B cells and T follicular helper cells in Sjögren’s disease. Cell Mol Immunol (2025). https://doi.org/10.1038/s41423-025-01346-y

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