Objective To explore the action mechanism and clinical significance of CD4+CD25+ regulatory T (Treg) cells in the development of atopic dermatitis (AD). Methods Peripheral blood mononuclear cells (PBMC) were obtained from 46 patients with AD and 20 normal human controls. Flow cytometry was performed to detect the number of CD4+CD25+ Treg cells, real-time fluorescence PCR assay to measure the Foxp3 mRNA level in PBMC, ELISA to determine the serum levels of IL-2, IL-4, IL-10 and IFN-γ. Results A statistical decrease was observed in the percentages of peripheral CD4+CD25+ Treg cells among CD3+ T cells and CD4+ T cells in AD patients compared with normal controls (t' = 3.775, 4.533, both P＜ 0.01 ), and in the percentage of peripheral CD4+CD25+ Treg cells among CD3+ T cells in patients with acute AD compared with those with chronic AD (t = 2.217, P ＜ 0.05), but no significant difference was noted between patients with acute AD and those with subacute AD or between those with subacute AD and those with chronic AD in the percentage of peripheral CD4+CD25+ Treg cells among CD3+ T cells (t = 1.558, 0.49, both P ＞ 0.05). The mRNA level of Foxp3 in PBMC from AD patients was statistically decreased compred with that from normal controls (z =-2.368, P ＜ 0.05 ). The count of CD4+CD25+ Treg cells was positively correlated with serum levels of IL-2 and IL-10 (r = 0.512, 0.494, both P ＜ 0.05), but had no significant correlation with serum levels of IL-4 and IFN-γ (r = -0.110, -0.237, both P ＞ 0.05). Conclusions In AD patients, there is a decrease in the count of CD4+CD25+ Treg cells and in the level of Foxp3 mRNA, which may suppress the proliferation of and secretion of Foxp3 mRNA by Th2 cells, lead to Th2 predominance, participate in the development of AD.

OBJECTIVE: To explore the toxicological mechanism of drug-induced liver injury(DILI) in rats induced by cantharidin(CTD). METHODS: SD rats were exposed to different doses of CTD(0.061 4, 0.092 1, 0.184 1 mg·kg−1) by oral gavage for 28 d. Liver index and serum liver function indictors were detected. HE staining was used to evaluate the pathological changes of liver. Then the proteins in endoplasmic reticulum stress(ERS), autophagy, and apoptosis-pathway were detected by Western blotting. RESULTS: The liver index was increased in CTD groups. The ALT, AST, LDH, ALP and T-Bil were increased by CTD with a dose-dependent manner. Disrupted hepatic architecture and dilatation of central vein were observed after CTD intervention. The protein expression levels of GRP78, CHOP, ATF4, Beclin-1, LC3, Caspase-3, Caspase-8, and Bax/Bcl-2 were increased after CTD intervention. Molecular docking results revealed that GRP78, ATF4, and Beclin-1 could directly interconnect with CTD. CONCLUSION CTD can activate ERS, autophagy and synergistically inducing downstream apoptosis in rat, providing a novel insight into the mechanism of CTD-induced DILI.