ABSTRACT
Objective To explore the role of CD4~+CD25~+CD127~(lo) regulatory T cells (Tregs) and inter-leukin (IL)-6, transforming growth factor beta (TGF-β), IL-17 in the pathogenesis of lupus nephritis (LN) by detecting the levels of IL-10, IL-6, TGF-β, IL-17, CD4~+CD25~+CD127~(lo) Tregs in the peripheral blood of patients with active and inactive LN. Methods Three-colour flow cytometry was used to quantitatively measure proportions of Treg cells, the levels of TGF-β, IL-17 were detected by ELISA, and the levels of IL-10, IL-6 in the peripheral blood were detected by Cytometric Bead Array System. Results ① Compared with the inactive LN and the normal controls (P<0.01), the level of CD4~+CD25~+CD127~(lo) Tregs from patients with active LN was lower(P<0.01). When compared with the normal controls, the level of CD4~+CD25~+CD127~(lo) Tregs from LN inactive patients had no significant difference (P>0.05). ② Compared with patients with inactive LN, the levels of IL-10, IL-6 was higher (P<0.01) in patients with active LN. ③ Compared with the patients with inactive LN and the normal controls, the levels of TGF-β, IL-17 was not significantly different (P>0.05). ④ The level of CD4~+CD25~+CD127~(lo) T cell was correlated negatively with the levels of IL-10, IL-6 and SLEDAI (P<0.05), and was not correlated with C3 and C4. ⑤ SLEDAI was correlated positively with the levels of IL-10 and IL-6 (P<0.01). SLEDAI and the level of IL-10 were correlated negatively with C3 and C4 (P<0.01 for both). ⑥ The level of CD4~+CD25~+CD127~(lo) Tregs from LN was not correlated with TGF-β and IL-17. ⑦ TGF-β was correlated positively with the level of IL-17. Conclusion ① The level changes of Tregs and IL-10, IL-6, TGF-β in the peripheral blood of LN can be used as the indicators for the activity status of lupus nephritis. ② Tregs and IL-10, IL-6 in the peripheral blood of LN patients is negatively correlated. ③ The glucocorticoid hormone is helpful to elevate the level of Tregs but decrease IL-17. T cell level can vary in different body status, different microenvironmental and immune status.