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Foxp3 expression in CD4+ T cells of patients with systemic lupus erythematosus (SLE): A comparative phenotypic analysis
  1. Michael Bonelli (michael.bonelli{at}meduniwien.ac.at)
  1. Department of Rheumatology, Internal Medicine III, Medical University of Vienna, Austria, Austria
    1. Karolina von Dalwigk (karolina.vondalwigk{at}meduniwien.ac.at)
    1. Department of Rheumatology, Internal Medicine III, Medical University of Vienna, Austria, Austria
      1. Anastasia Savitskaya (anastasia.savitskaya{at}meduniwien.ac.at)
      1. Department of Rheumatology, Internal Medicine III, Medical University of Vienna, Austria, Austria
        1. Josef S Smolen (josef.smolen{at}wienkav.at)
        1. Department of Rheumatology, Internal Medicine III, Medical University of Vienna, Austria, Austria
          1. Clemens Scheinecker (clemens.scheinecker{at}meduniwien.ac.at)
          1. Department of Rheumatology, Internal Medicine III, Medical University of Vienna, Austria, Austria

            Abstract

            Objectives: The forkhead family transcription factor Foxp3 currently represents the most specific marker molecule for CD4+CD25+ T cells with suppressive/regulatory capacity (Treg) in the mouse. Recent studies in the human system, however, indicate that the expression of Foxp3 can be T cell activation dependent. This tempted us to evaluate the significance of Foxp3 expression under autoimmune conditions with chronic T cell activation in SLE patients as compared to healthy controls (HC).

            Methods: Proportions of peripheral blood CD4+Foxp3+ T cells and CD4+CD25high T cells were determined in active and inactive SLE patients as compared to HC by flow cytometry. Comparative analysis of the % of CD4+Foxp3+ T cells and of % of CD4+CD25high T cells with clinical disease activity and T cell activation marker molecule expression were performed. Finally, the induction of Foxp3 expression was analyzed upon T cell activation in vitro.

            Results: Proportions of CD4+Foxp3+ T cells were significantly increased in SLE patients as compared to HC and a significant correlation was observed between clinical disease activity and proportions of CD4+Foxp3+ T cells. On the other hand, proportions of CD4+CD25high were decreased in SLE and no correlation with a T cell activation marker expression of was observed. In addition, in vitro activation of T cells induced Foxp3 expression.

            Conclusions: Our data suggest that the expression of Foxp3 on CD4+ T cells in SLE patients, at least to some extent, reflects the activation of CD4+ T cells due to underlying disease activity and does not necessarily indicate a functional regulatory T cell capacity.

            • Foxp3
            • SLE
            • T-cell activation
            • regulatory T cells
            • systemic lupus erythematosus

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