Myeloid‐Derived Suppressor Cell–Derived Interferon‐β Promotes T Follicular Helper Cell Response and Exacerbates Lupus Development
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Le résumé fourni par la source
Objective Increasing evidence highlights a critical role of T follicular helper (Tfh) cells in autoimmune pathogenesis. This study aimed to identify inflammatory cytokines involved in driving Tfh cell responses in systemic lupus erythematosus (SLE). Methods The circulating Tfh frequencies and interferon (IFN)‐β levels were analyzed for correlations with disease activities in patients with SLE. Both lupus mice with IFN‐β treatment and Ifnar1 −/− mice with lupus induction were assessed for Tfh cell responses and disease progression. Sorting‐purified naive CD4 + T cells from Ifnar1 −/− mice were adoptively transferred to lupus mice for monitoring Tfh cell differentiation in vivo. In culture, mouse CD4 + T cells treated with IFN‐β were examined for Tfh cell differentiation and intracellular signaling pathway. The underlying mechanism for IFN‐β secretion by myeloid‐derived suppressor cells (MDSCs) was investigated by co‐immunoprecipitation and Western blotting. Results We found that increased Tfh cells with IFN‐I–inducible gene signatures correlated with disease activities in patients with SLE. Consistently, IFN‐β treatment markedly enhanced Tfh cell response and exacerbated disease progression in lupus mice. Moreover, mice with IFNAR1 deficiency exhibited attenuated lupus progression with significantly decreased Tfh response. Mechanistically, IFN‐β activated the indoleamine 2,3‐dioxygenase/kynurenine/aryl hydrocarbon receptor (IDO/Kyn/AhR) axis to promote Tfh cell differentiation. Notably, expanded MDSCs in lupus were found to produce high levels of IFN‐β. Further studies showed that the autoantigen activated lymphocyte‐derived DNA stimulated IFN‐β production by MDSCs via the cyclic GMP‐AMP synthase–stimulator of IFN genes (cGAS‐STING)–dependent pathway. Conclusion These results have demonstrated a novel function of IFN‐β in promoting Tfh cell response during lupus progression, which may facilitate the identification of new therapeutic targets for the treatment of SLE. image
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Myeloid‐Derived Suppressor Cell–Derived Interferon‐β Promotes T Follicular Helper Cell Response and Exacerbates Lupus Development
- Date Crossref
- 11/02/2026
- Éditeur
- Wiley
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Jiangsu University Department of Laboratory Medicine pays non établi dans la noticeUniversité ou école supérieure
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Affiliated Hospital of Jiangsu University pays non établi dans la noticeÉtablissement de santé
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China Three Gorges University pays non établi dans la noticeUniversité ou école supérieure
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Chinese University of Hong Kong pays non établi dans la noticeUniversité ou école supérieure
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Hong Kong Science and Technology Parks Corporation pays non établi dans la noticeOrganisation à but non lucratif
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University of Hong Kong Department of Pathology pays non établi dans la noticeUniversité ou école supérieure
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Soochow University Institute of Biology and Medical Sciences pays non établi dans la noticeUniversité ou école supérieure
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Authorship note: Ke Rui pays non établi dans la noticeInstitution
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School of Medicine Department of Immunology pays non établi dans la noticeUniversité ou école supérieure
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Department of Rheumatology The Second People's Hospital of Three Gorges University Yichang China Department of Rheumatology pays non établi dans la noticeUniversité ou école supérieure
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Faculty of Medicine Department of Pathology pays non établi dans la noticeUniversité ou école supérieure
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School of Biology and Basic Medical Sciences Institute of Biology and Medical Sciences pays non établi dans la noticeUniversité ou école supérieure
Department of Laboratory Medicine — Jiangsu University, Affiliated Hospital of Jiangsu University et China Three Gorges University, avec 9 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.