Role of immune tolerance in BALB/c mice with anaphylactic shock after Echinococcus granulosus infection.

This study tested the hypothesis that immune tolerance mediated by regulatory T (Treg) cells is protective against cystic echinococcosis (CE)-induced anaphylactic shock. BALB/c mice were inoculated with protoscoleces of Echinococcus granulosus. After 3 months, the presence of cysts in the peritoneal cavity was confirmed after which a subset of mice was sensitized using a cyst fluid suspension to induce anaphylactic shock. While IgE levels were significantly higher in both groups inoculated with E. granulosus as compared to the healthy control group (both P < 0.01), sensitized mice had higher IgE levels as compared with those with E. granulosus alone (P < 0.05). Mice inoculated with E. granulosus alone and sensitized mice both had significantly higher histamine levels as compared to the healthy controls. The proportion of CD4(+)CD25(+)Foxp3(+) Treg cells relative to CD4(+) cells was significantly higher in mice inoculated with E. granulosus alone (P < 0.0167); significantly higher interleukin-10 (IL-10) and tumor growth factor-ß (TGF-ß1) levels were also noted in this group (all P < 0.01). In contrast, IL-13 and IL-17A levels were significantly higher in the sensitized mice (both P < 0.05). Taken together, these data suggest that the biphasic changes in Treg cell and cytokine levels may be associated with anaphylactic shock induced by CE.

Transmembrane protein 166 expression in esophageal squamous cell carcinoma in Xinjiang, China.

OBJECTIVE: Transmembrane protein 166 (TMEM166) expression in esophageal squamous cell carcinoma (ESCC) and remote normal esophageal tissues was examined to assess any role in tumour biology. METHODS: TMEM166 mRNA expression in 36 cases with ESCC (36 tumour samples, 36 remote normal esophageal tissue samples) was detected by RT-PCR. TMEM166 protein expression was analysed in paraffin-embedded tissue samples from the same cases by immunohistochemistry. RESULTS: Semi-quantitative analysis showed TMEM166 mRNA expression in ESCCs to be significantly lower than in remote normal esophageal tissues (0.759 ± 0.713 vs. 2.622 ± 1.690, P=0.014). TMEM166 protein expression was also significantly reduced (69.4% vs. 94.4%, P<0.01). CONCLUSION: TMEM166 mRNA and protein expression demonstrated significant reduction in ESCCs compared with remote esophageal tissues, albeit with no correlation with tumour size, differentiation, stage, and lymph node metastasis, suggesting a role in regulating autophagic and apoptotic processes in the ESCC.

[Regulation on phenotypic and functional maturation of dendritic cells by apolipoprotein A-I].

AIM: to investigate the effects of apolipoprotein A-I (ApoA-I) on the peripherial blood dendritic cell (PBDC) and monocyte derived DC (MDDC) in vitro. METHODS: isolate PBDC or monocyte by cell isolation kit, monocyte were induced to MDDC by treated with GM-CSF plus IL-4 for 6 days, and then collect PBDC and MDDC treated them with apoA-I, LPS or TNF-α for 24 hours. Then check the cell surface marker and phagocytic capacity by flow cytometry. ELISA was used to detect the levels of cytokine secretion. T cells were stained with CFSE and T cell proliferation was assessed by flow cytometry. RESULTS: collect the PBDC and MDDC with high purity. In the presence of ApoA-I, the surface markers on MDDC, such as CD40, CD86 and MHC-II, were up-regulated which were detected by flow cytometry. CD83 expression on both PBDC and MDDC was remarkably increased. ApoA-I DC demonstrated decreased the phagocytic capacity. ApoA-I also stimulated MDDC to produce IL-12 and TNF-α. Furthermore, ApoA-I can induce considerable Th cell proliferation. CONCLUSION: ApoA-I can induce the maturation and activation of MDDC and PBDC, including the cytokine secretion, specific antigen presentation and T cell proliferation and decreasing the phagocytic capacity. Therefore, ApoA-I may attribute to the immune response in AS process.