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Circulating cytokines in active Polymyalgia Rheumatica
  1. Lorena Alvarez-Rodríguez
  1. Servicio Reumatología. Hospital Universitario Marqués de Valdecilla, Spain
    1. Marcos Lopez-Hoyos (inmlhm{at}humv.es)
    1. Servicio Inmunología. Hospital Universitario Marqués de Valdecilla, Spain
      1. Cristina Mata
      1. Servicio Reumatología. Hospital Sierrallana, Spain
        1. María J Marín
        1. Servicio Reumatología. Hospital Universitario Marqués de Valdecilla, Spain
          1. Jaime Calvo-Alen
          1. Servicio Reumatología. Hospital Sierrallana, Spain
            1. Ricardo Blanco
            1. Servicio Reumatología. Hospital Universitario Marqués de Valdecilla, Spain
              1. Elena Aurrecoechea
              1. Servicio Reumatología. Hospital Sierrallana, Spain
                1. María Ruiz-Soto
                1. Servicio Reumatología. Hospital Universitario Marqués de Valdecilla, Spain
                  1. Víctor M Martínez-Taboada (vmartinezt{at}medynet.com)
                  1. Servicio Reumatología. Hospital Universitario Marqués de Valdecilla, Spain

                    Abstract

                    Objective: To characterize the circulating cytokine profile and the cellular source of circulating cytokines in polymyalgia rheumatica (PMR).

                    Methods: The study included 34 patients with active untreated PMR and 17 age-matched healthy controls (HC). Circulating cytokines were measured by CBA and ELISA. Intracellular cytokines were assessed in CD3+ and CD14+ cells by flow cytometry. Cytokines in cell culture supernatants were also determined after polyclonal stimulation of patient’s PBMC.

                    Results: Circulating levels of IL-6 were significantly higher in active PMR compared to HC. Corticosteroid (CS) treatment was followed by a decrease of IL-6. Intracellular cytokine staining showed that circulating monocytes did not produce higher amounts of proinflammatory cytokines in PMR patients than in HC. There was a discordance between serum levels and cytokine-producing monocyte and T cells and we were not able to demonstrate a Th1 bias in the peripheral compartment.

                    Conclusion: Active PMR is characterized by increased serum levels of IL-6, but not of other pro-inflammatory cytokines, that are rapidly suppressed by CS therapy. Probably, as circulating monocytes do not show increased production of proinflammatory cytokines, IL-6 might be mainly produced in the inflamed tissue. The study of the circulating cytokine profile and its cellular source may provide a clue to new therapeutic options.

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