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Questions {❓}

• Is it citrullinated epitopes of specific proteins, and if so, where are these epitopes most influential?
• The therapeutic window of opportunity in rheumatoid arthritis: does it ever close?
• This raises compelling questions: Do these changes reflect a therapeutic effect, or might they indicate a continuum of disease progression?

Schema {🗺️}

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         description:Rheumatoid arthritis (RA) is a complex autoimmune disease characterized by chronic inflammation of the synovial tissue, where T cells play a central role in pathogenesis. Recent research has identified T peripheral helper (Tph) cells as critical mediators of local B cell activation in inflamed tissues. This review synthesizes the latest advancements in our understanding the of the role of T cells in RA, from initiation to established disease. We explore recent advances regarding the genetic and epigenetic factors that predispose individuals to RA, the mechanisms of T cell activation and differentiation, and the interactions between T cells and other immune and stromal cells within the synovial microenvironment. The emergence of Tph cells as key drivers of RA pathobiology is highlighted, along with their potential as therapeutic targets. We also discuss the heterogeneity of T cell responses and their interplay with synovial cells, while addressing critical research gaps such as the drivers of T cell recruitment and the plasticity of synovial phenotypes. A deeper understanding of T cell dynamics in RA will provide valuable insights for developing targeted therapies to modulate T cell-mediated inflammation and improve patient outcomes.
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      headline:T Cell Dysregulation in Rheumatoid Arthritis: from Genetic Susceptibility to Established Disease
      description:Rheumatoid arthritis (RA) is a complex autoimmune disease characterized by chronic inflammation of the synovial tissue, where T cells play a central role in pathogenesis. Recent research has identified T peripheral helper (Tph) cells as critical mediators of local B cell activation in inflamed tissues. This review synthesizes the latest advancements in our understanding the of the role of T cells in RA, from initiation to established disease. We explore recent advances regarding the genetic and epigenetic factors that predispose individuals to RA, the mechanisms of T cell activation and differentiation, and the interactions between T cells and other immune and stromal cells within the synovial microenvironment. The emergence of Tph cells as key drivers of RA pathobiology is highlighted, along with their potential as therapeutic targets. We also discuss the heterogeneity of T cell responses and their interplay with synovial cells, while addressing critical research gaps such as the drivers of T cell recruitment and the plasticity of synovial phenotypes. A deeper understanding of T cell dynamics in RA will provide valuable insights for developing targeted therapies to modulate T cell-mediated inflammation and improve patient outcomes.
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