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Objective: To investigate the contribution of T lymphocytes and monocytes to cytokine production in systemic lupus erythematosus (SLE).Methods: Forty-five SLE patients and 19 healthy volunteers were included. Serum levels of tumor necrosis factor alpha (TNFa), interferon gamma (IFNc), interleukin (IL)-6, and IL10 were quantified by ELISA. The cytokine production capacities of peripheral blood mononuclear cells were assessed by culturing in vitro with PMA1Ionomycin or LPS. The intracellular cytokine expression was measured by flow cytometry in T lymphocytes and monocytes, respectively. The influence of the disease activity (measured as the SLE-disease activity index; SLEDAI) and the treatment the patients were receiving was evaluated.Results: Serum IL10, IL6, and TNFa levels were increased in patients (P ≤ 0.01), and a higher spontaneous (without stimuli) intracellular expression of IL10 in CD41 and CD81 T lymphocytes (P < 0.05) and of IL6 in monocytes (P 5 0.01) were found. After stimulation, patients presented a higher percentage of CD41 and CD81 T lymphocytes producing IL4 and IL10 (P ≤ 0.01), and of monocytes producing IL6 (P 5 0.04) and IL10 (P 5 0.008). The SLEDAI score was positively correlated with the percentage of CD41IL101 and CD81IL101 T lymphocytes (P < 0.01), and inversely correlated with CD81TNFa1 (P 5 0.02), CD41IFNg1 (P 5 0.04) and CD81 IFNg1 (P 5 0.002) T lymphocytes. Patients receiving high dose prednisone produced higher IL10, but they also were the patients with a more active disease.Conclusion: Monocytes and T lymphocytes (CD41 and CD81) contribute to an overproduction of IL6 and IL10 in SLE; this correlates with the disease activity but is independent of the treatment the patients are receiving. q 2009 Clinical Cytometry Society

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MetS may contribute to the development of atherosclerosis by significantly increasing inflammation levels and arterial stiffness and decreasing circulating EPCs. This finding would justify close monitoring of these patients.