@article {L{\'O}PEZ1559, author = {PATRICIA L{\'O}PEZ and JES{\'U}S G{\'O}MEZ and CATUXA PRADO and CARMEN GUTI{\'E}RREZ and ANA SU{\'A}REZ}, title = {Influence of Functional Interleukin 10/Tumor Necrosis Factor-α Polymorphisms on Interferon-α, IL-10, and Regulatory T Cell Population in Patients with Systemic Lupus Erythematosus Receiving Antimalarial Treatment}, volume = {35}, number = {8}, pages = {1559--1566}, year = {2008}, publisher = {The Journal of Rheumatology}, abstract = {Objective As interleukin 10 (IL-10)/tumor necrosis factor-α(TNF-α) polymorphisms have been shown to influence TNF-α inhibition and clinical response to antimalarial treatment in patients with systemic lupus erythematosus (SLE), we investigated involvement of these variants in antimalarial effects on cytokine serum levels and regulatory T cell population (Treg). Methods The alleles present at -308 TNF-α and-1082 IL-10 genes; serum concentrations of inter-feron-α (IFN-α), IL-10 and TNF-α; and size and function of CD4+CD25high (Treg) population were determined in SLE patients and in healthy controls. These data were related to treatment and clinical manifestations. Results Patients were observed to have increased IFN-α serum levels that did not correlate with any treatment. Among patients receiving antimalarial drugs, high IL-10/low TNF-α producers presented higher levels of IFN-α and IL-10 than carriers of other genotypes. In contrast, patients with the converse, low IL-10/high TNF-α genotype who were receiving antimalarial treatment presented increased size and function of Treg population. The percentage of CD4+CD25high cells was inversely correlated to TNF-α levels. Conclusion Our findings suggest that the beneficial effect of antimalarials in low IL-10/high TNF-α patients with SLE may be partially attributable to the increase in Treg activity, whereas patients with the converse genotype did not show this phenomenon, yet did have significantly upregulated levels of IFN-α and IL-10, 2 cytokines that have been associated with SLE activity.}, issn = {0315-162X}, URL = {https://www.jrheum.org/content/35/8/1559}, eprint = {https://www.jrheum.org/content/35/8/1559.full.pdf}, journal = {The Journal of Rheumatology} }