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cookies, bmc, privacy, data, cia, mice, group, erastin, page, analysis, treated, contact, function, optional, content, personal, parties, policy, information, manage, journal, translational, medicine, submission, inflammatory, antigen, presenting, staining, joint, fer, gsk, article, enquiries, editing, authors, choice, essential, make, site, advertising, personalisation, usage, social, media, accepting, consent, processing, including, transfers, european,

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article page journal erastin + gsk484 = cia mice treated erastin = cia mice treated fer-1 = cia mice treated pbs = cia mice group authors scientific editing privacy choices/manage cookies bmc european economic area translational medicine home antigen presenting function synovial bone erosion nc = normal control dot plot represents hind knee joint representative immunohistochemical staining state privacy rights accepting optional cookies click contact manage preferences gsk484 group 1479-5876 contact submission enquiries erastin group fer-1 group personal data optional cookies essential cookies cookies skip account journal eosin staining joint inflammation cookies policy privacy policy privacy statement data protection usage analysis social media varying standards ferrostatin-1 reduces inflammatory response rheumatoid arthritis synoviocytes effects citrullinated antigens inflammatory factors histological scores cit-h3 tnf-α ifn-γ quantitative analysis

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         headline:Ferrostatin-1 reduces the inflammatory response of rheumatoid arthritis by decreasing the antigen presenting function of fibroblast-like synoviocytes
         description:Rheumatoid arthritis (RA) is a systemic chronic autoimmune disease with complex mechanism. Currently, ferroptosis is believed to play a role in it, but the specific mechanism is unknown, especially in immune response. In this study, we demonstrated that the high expression of major histocompatibility complex I (MHC-I) molecules in RA fibroblast-like synoviocytes (FLSs) is an antigen-presenting cell property and that this property is closely related to the increase in antigens after citrullination. Moreover, we detected higher levels of ferroptosis among FLSs from RA patient than among FLSs from OA patients. Ferroptosis can increase the expression of citrullinated histone H3 (cit-h3) by promoting the production of peptidyl arginine deiminase 4 (PAD4), which further promotes the expression of MHC-I molecules. We cocultured RA-FLSs treated with ferroptosis drugs with selected CD8 + T cells to assess the effect of ferroptosis on the endogenous antigen-presenting function of RA-FLSs. Ferroptosis promoted the proliferation of CD8 + T cells and the release of the inflammatory factors Tumor necrosis factor-α (TNF-α) and Interferon-gamma (IFN-γ), which enhanced the inflammatory effect. This phenomenon was also observed in a collagen-induced arthritis (CIA) mouse model. Finally, ferrostatin-1 (fer-1), a ferroptosis inhibitor, inhibited the above effects and reduced the release of inflammatory factors, indicating that ferroptosis may play a therapeutic role in RA and providing new ideas for the treatment of RA in the field of immunity.
         datePublished:2025-03-06T00:00:00Z
         dateModified:2025-03-06T00:00:00Z
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            Rheumatoid arthritis
            Ferroptosis
            Immune
            Antigen presentation
            Inflammation
            Biomedicine
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      headline:Ferrostatin-1 reduces the inflammatory response of rheumatoid arthritis by decreasing the antigen presenting function of fibroblast-like synoviocytes
      description:Rheumatoid arthritis (RA) is a systemic chronic autoimmune disease with complex mechanism. Currently, ferroptosis is believed to play a role in it, but the specific mechanism is unknown, especially in immune response. In this study, we demonstrated that the high expression of major histocompatibility complex I (MHC-I) molecules in RA fibroblast-like synoviocytes (FLSs) is an antigen-presenting cell property and that this property is closely related to the increase in antigens after citrullination. Moreover, we detected higher levels of ferroptosis among FLSs from RA patient than among FLSs from OA patients. Ferroptosis can increase the expression of citrullinated histone H3 (cit-h3) by promoting the production of peptidyl arginine deiminase 4 (PAD4), which further promotes the expression of MHC-I molecules. We cocultured RA-FLSs treated with ferroptosis drugs with selected CD8 + T cells to assess the effect of ferroptosis on the endogenous antigen-presenting function of RA-FLSs. Ferroptosis promoted the proliferation of CD8 + T cells and the release of the inflammatory factors Tumor necrosis factor-α (TNF-α) and Interferon-gamma (IFN-γ), which enhanced the inflammatory effect. This phenomenon was also observed in a collagen-induced arthritis (CIA) mouse model. Finally, ferrostatin-1 (fer-1), a ferroptosis inhibitor, inhibited the above effects and reduced the release of inflammatory factors, indicating that ferroptosis may play a therapeutic role in RA and providing new ideas for the treatment of RA in the field of immunity.
      datePublished:2025-03-06T00:00:00Z
      dateModified:2025-03-06T00:00:00Z
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         Rheumatoid arthritis
         Ferroptosis
         Immune
         Antigen presentation
         Inflammation
         Biomedicine
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         Medicine/Public Health
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      name:Juan Zhang
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            address:
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      name:Haoyuan Sun
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               type:PostalAddress
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      name:Yanlei Ge
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      name:Department of Rheumatology, First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Rheumatology, First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Rheumatology, First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Rheumatology, First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Rheumatology, First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Rheumatology, First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Osteology, Heilongjiang Provincial Hospital, Harbin, China
      name:Department of Respiratory Medicine, North China University of Science and Technology Affiliated Hospital, Tangshan, China
      name:Department of Rheumatology, First Affiliated Hospital of Harbin Medical University, Harbin, China

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