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FOXP3 expression in blood, synovial fluid and synovial tissue during inflammatory arthritis and intra-articular corticosteroid treatment
  1. S Raghavan (sukanya.raghavan{at}
  1. Karolinska Insitutet, Sweden
    1. D Cao (duojia.cao{at}
    1. Karolinska Insitutet, Sweden
      1. M Widhe (mona.widhe{at}
      1. Karolinska Insitutet, Sweden
        1. K Roth (katrin-roth{at}
        1. Karolinska Insitutet, Sweden
          1. J Herrath (j.herrath{at}
          1. Karolinska Insitutet, Sweden
            1. M Engström (marianne.engstrom{at}
            1. Karolinska Insitutet, Sweden
              1. G Roncador
              1. Centro Nacional de Investigaciones Oncologicas, Spain
                1. A H Banham (alison.banham{at}
                1. University of Oxford, United Kingdom
                  1. C Trollmo (tina.trollmo{at}
                  1. Karolinska Insitutet, Sweden
                    1. A I Catrina (anca.catrina{at}
                    1. Karolinska Insitutet, Sweden
                      1. V Malmström (vivianne.malmstrom{at}
                      1. Karolinska Insitutet, Sweden


                        Objective: To analyse the distribution of FOXP3+CD25+CD4+ regulatory T cells (Treg) in peripheral blood, synovial fluid and tissue of patients with rheumatic disease during relapse and following local treatment.

                        Methods: FOXP3 expression was assessed by flow cytometry, immunohistochemistry, immunofluorescence and real-time polymerase chain reaction (RT-PCR). The functional suppressive capacity of Treg was analyzed following co-culture with effector CD4+CD25- T cells through assessment of proliferation and cytokine secretion.

                        Results: We demonstrate that FOXP3 protein and mRNA expression in synovial fluid T cells was not confined solely to CD25bright T cells as seen in blood, but included CD25intermediate and even CD25neg T cells. Indeed, synovial fluid CD25high T cells showed similar suppressive capacity as CD25bright T cells indicating presence of functional Treg in T cells with lower intensity of CD25. In synovial tissue, FOXP3+ cells were present in low numbers within T cell infiltrates and decreased further following intraarticular glucocorticosteroid administration in parallel with the general reduction in inflammation.

                        Conclusions: Identification of synovial fluid FOXP3+ Treg with varying intensities of CD25 opens up possibilities for thorough characterization of this important T cell subset in the inflammatory compartment. However, only scarce synovial membrane expression of FOXP3 was found even in the absence of overt inflammation, suggesting that the synovial membrane is a site that would benefit therapeutically from Treg expansion.

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