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Keywords {🔍}

ferroptosis, cells, article, pubmed, raflss, arthritis, pad, google, scholar, expression, erastin, group, cas, cell, fer, synovial, inflammatory, fig, levels, rheumatoid, patients, flss, cia, mice, citrullinated, data, antigen, results, inflammation, analysis, joint, gsk, central, role, presentation, function, antigenpresenting, factors, protein, flow, effect, control, increased, cytometry, response, disease, study, cith, treated, model,

Topics {✒️}

circhipk3/mir-149-5p/foxo1/vegf functional module disease-modifying anti-rheumatic drugs author information authors rheumatism collaborative initiative additional information publisher nf-κb/mapk signaling electronic supplementary material exhibit antigen-presenting functions antigen presentation-induced inflammation endogenous antigen-presenting function goat anti-rabbit igg erastin + gsk484 = cia mice treated antigen-presenting cell phenotype 10% sds‒page antigen-presenting cell property type ii collagen-stimulated representative micro-computed tomography anti-citrullinated protein antibodies authors scientific editing springer nature state privacy rights conclusions ferroptosis van der heijde privacy choices/manage cookies activating mhc-ii-restricted endogenous antigen presentation erastin = cia mice treated immune-mediated disease peripheral blood collection providing additional support fer-1 = cia mice treated endogenous antigen presenting bmc underwent joint replacement facilitating antigen presentation antigen presentation function pbs = cia mice group enhancing antigen presentation iron-dependent form citrullinated histone h3 inflammatory cell infiltration serum igg antibodies antigen presenting function antigen-presenting function cia mouse models paw thickness evaluated key autoimmunity-related enzymes detected higher levels inflammatory factor protein specific methods

Questions {❓}

• However, how does ferroptosis trigger the upregulation of PAD enzyme expression?

Schema {🗺️}

WebPage:
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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.
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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.
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      dateModified:2025-03-06T00:00:00Z
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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
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      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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