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 Printable version |
Prolonged standard treatment for systemic lupus erythematosus fails to normalize the secretion of innate immunity-related chemokines |
European Cytokine Network. Volume 21, Number 1, 71-6, March 2010, Research article
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 Free Article
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Author(s) : Luisa Vega, Julia Barbado, Raquel Almansa, Rocío González-Gallego, Lucía Rico, Antonio Jimeno, Mercedes Nocito, Raúl Ortiz de Lejarazu, Jesus F Bermejo-Martin |
Summary : The pathogenesis of systemic lupus erythematosus (SLE) is far from having been elucidated at the molecular level. Using a multiplex system, we profiled 18 immune mediators in the plasma from 57 patients with SLE. Thirteen of them showed mild to moderate disease activity, and 29 showed severe activity, based upon the SLEDAI score. Fifteen patients were in complete clinical remission. Those patients with active disease, and those in clinical remission had been undergoing immunomodulatory treatment for an average of 10.7 months and 19.2 months respectively at the time of the visit. Samples obtained from 10 healthy volunteers were used as control. Patients with active disease and those with inactive disease showed elevated levels of the chemoattractant proteins MCP-1/CCL2, MIP1-β/CCL4 and IL-8/CXCL8 as compared to the control (p <\; 0.05). This pattern of increased mediator levels was observed regardless of the immunomodulatory drug regimen received (non-steroidal anti-inflammatory, steroids or immunosuppressants), and of the degree of tissue damage. Patients with anticardiolipin antibodies (ACAs) showed significantly higher levels of IL-8 and MIP-1β than those with no ACAs. Levels of MCP-1/CCL2, MIP1-β/CCL4 and IL-8/CXCL8 correlated significantly, indicating a coordinated regulation of their secretion. Conversely, levels of Th1, Th2, Th17 cytokines, IFN-γ and growth factors did not differ from those found in the healthy controls. IFN-α, IL-1β, IL-6, IL-7 and IL-13 were undetectable. In conclusion, long term treatment of SLE with standard immunomodulatory drug regimens fails to normalize levels of key chemoattractant proteins linked to innate immunity. This might suggest the existence of a basal, pro-inflammatory state in patients with lupus, even in the absence of symptoms, which could serve as a “substratum” or initiator of the immunological events taking place during a flare-up of the disease. |
Keywords : ACAs, anticardiolipin antibodies, G-CSF, granulocyte colony-stimulating factor, GM-CSF, granulocyte macrophage colony-stimulating factor, IFN-γ, interferon γ, MCP-1, monocyte chemoattractant protein-1, MIP-1α, macrophage inflammatory protein-1α, MIP-1β, macrophage inflammatory protein-1β, PBMCs, peripheral blood mononuclear cells, SLE, systemic lupus erythematosus, TNF-α, tumor necrosis factor α |
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