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Background – Aim: Loss of tolerance to self-antigens repre sents the critical factor for pathogenesis initiation in systemic lupus erythematosus (SLE) and lupus nephritis (LN). T regulatory cells (Tregs) and related cytokines (IL-6, IL-10, TGF-β1) are the main mediators of this mechanism. The aim of this study was the evaluation of Tregs and IL-6, IL-10 and TGF-β1 in the course of LN patients. Patients – Methods: Twenty LN patients (18 female, 2 male, mean age 33.8±8.8 years, mean disease duration 87.2±63.4 months) were included; twelve with a histological diagnosis (10 class IV+V, 2 class V). CD4+CD25highFOXP3+ Tregs were analyzed in 61 samples (44 active, 17 quiescent disease). IL-6, IL-10 and TGF-β1 were evaluated in 18 patients (10 active, 8 inactive LN). Disease activity was evaluated with SLE Disease Activity Index (SLEDAI). Other parameters included C3/C4d complement fragments, antidsDNA antibodies and proteinuria. Analysis was performed with Kruskal-Wallis test; p<0.05 was considered significant. Results: Tregs were significantly lower in active LN (0.71±0.29% vs. 1.14±0.19% of the CD4+ T cells, p<0.001). IL-6 and IL-10 were significantly higher (IL-6: 6.25±2.38 vs. 1.62±1.66pg/ml, p<0.001, IL-10: 5.8±3.8 vs. 1.7±2.6pg/ml, p=0.025), whereas TGFβ1 was lower (16529±7962 vs. 25957±6776pg/ml, p=0.034) in active LN. C3 and C4d were significantly lower in active disease (C3: 82.1±22.3 vs. 152±29.9mg/dl, p<0.001 and C4d: 8.7±4.3 vs. 21±7.7mg/dl, p<0.001). Conclusions: Tregs and TGF-β1 were significantly lower in active LN, while IL-6 and IL-10 were detected in higher levels. Impairment of IL-6/TGF-β1 axis seems to drive Tregs reduction in active LN; on the contrary, IL-10, despite its known regulatory profile, seems to exert mainly proinflammatory functions in LN.

IMMUNE REGULATION IN LUPUS NEPHRITIS: ROLE OF CD4+CD25high FOXP3+ T REGULATORY CELLS AND RELATED CYTOKINES (IL-6, IL-10, TGF�)