Atherosclerosis (AS) is a complicated arterial disease resulting from abnormal lipid deposition and inflammatory injury, which is attributed to Yin deficiency, accumulation of heat materials, and stasis of blood flow in Traditional Chinese Medicine (TCM) theory. Thus, according to TCM theory, the method of nourishing Yin (Yangyin), clearing away heat (Qingre), and promoting blood circulation (Huoxue) is a reasonable strategy, which has achieved remarkable clinical efficacy in the treatment of AS, but the mechanisms remain to be known. In this study, we evaluated the effects of Yangyin Qingre Huoxue Prescription (YQHP) on AS in ApoE-/- mice suffering from a high-fat diet and heat shock protein (HSP65) attack. YQHP regulated levels of blood lipids and inflammation-linked cytokines as well as Th17/Treg ratio in peripheral blood. Suppressed IL-6-p-STAT3 signaling and restored IL-2-p-STAT5 signaling in the presence of YQHP may partake in the regulation of Th17 and Treg differentiation. Moreover, YQHP modulated transcriptional levels of costimulator CD80 in aortas as well corresponding to the downregulation of GM-CSF in serum and CD3 expression in CD4+ T cells, which might indicate the potential of YQHP to regulate antigen presenting cells. All these effects eventually promoted the improvement of atherosclerotic lesions. In addition, YQHP promoted less monocyte infiltration in the liver and lower levels of AST, ALT, and AKP production than simvastatin. Conclusively, lipid-regulating and anti-inflammatory functions mediated by YQHP with lower hepatotoxicity than simvastatin hindered the progression of HSP65 aggravated AS in ApoE-/- mice, indicating the effectiveness of Yangyin Qingre Huoxue Method in the treatment of AS.

This study aims to observe the pathological changes of the brain and spinal cord in an experimental allergic encephalitis (EAE) mice model in the early onset, peak and remission periods of the disease, to detect the changes in the T-cell subsets and cytokine levels, to analyze the types of immune response and related principles in the different stages of the disease.
C57BL/6 mice were randomly divided into two groups: the EAE group (n = 18) and the control group (n = 18). C57BL/6 mice were immunized with myelin oligodendrocyte glycoprotein (MOG) 35-55 polypeptide/complete Freund's adjuvant (CFA) to establish the EAE mouse model. In the control group, the mice were treated with normal saline. The weights of the mice were recorded during the experiment. Peripheral blood was collected on the 0 day, 3rd day, 7th day, 14th day and 21st day after immunization, and the levels of T-cell subsets were detected by flow cytometry. The brain and spinal cord were taken on the 7th day (early onset), 18th day (peak) and 30th day (remission) after immunization. HE staining was used to observe the infiltration of inflammatory cells, and LFB staining was used to observe the loss of the myelin sheath. The immunohistochemical method was used to detect the T cells and B cell related proteins, and an ELISA assay was used to detect the changes of IL-4, IL-6, IL-10, IL-12, IL-17, IL-23, TNF-α, IFN-γ and TGF-β in mouse brain tissue. The interactions between the T cell subsets and cytokines, the types of immune responses of the EAE mice in different stages of the disease, and their related principles were analyzed.
The symptoms of the EAE mice after treatment for 18 d were more severe than those at 7 d in the mice, while the symptoms were significantly relieved at 30 d. These findings coincide with the results of the weight measurement in mice. The immunohistochemical detection of T-cell and B-cell subset related factors showed that T cells accumulated in the brains of the EAE mice. In contrast, there was no obvious aggregation of B cells. The Th17 and Th2 levels in the T cell subsets in the EAE group were higher than those in the control group from the beginning of the treatment to the twenty-first day after the treatment. The level of Th1 in the EAE group was higher than it was in the control group on the seventh day after the treatment, and it was lower during the rest of the time than it was in the control group. There was no significant difference in the level of γδT between the control group and the EAE group. ELISA results showed that the cytokines in the EAE group were higher than they were in the control group on the seventh day after treatment, but the levels of IFN-γ, IL-12, TGF-β, and IL-23 in EAE group were lower than they were in the control group on the 18th day after the treatment. There was no significant difference in the levels of cytokines between the two groups on the 30th day after the treatment.
At the different disease stages of the EAE mice, the balance between Th1 and Th2 and the balance of Th17 differentiation changed. Th17 promoted the development of the disease, and Th2 was more effective in restoring health.
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γδ T cells play an important role in infectious, autoimmune, or neoplastic diseases. Here, a study was conducted to investigate the dynamic changes in phenotype and function of peripheral γδ T cells in patients with chronic hepatitis B (CHB) during pegylated-interferon (pegIFN)-α treatment, and to explore their roles in IFN-α therapy.
Total 15 CHB patients with pegIFN-α therapy and 6 healthy controls (HC) were enrolled in this study. Flow cytometry was used for the study of frequency of peripheral γδ T cells, subtypes, effector or memory γδ T cells, and also the IFN-γ+, TNF-α+, CD107a+ or Granzyme B+ γδ T cells in 10 patients at week 0, 4, 8, 12, 24, 36 and 48 of treatment. Another 5 CHB patients and 6 HC were recruited for the γδ T cell isolation, and gene expression in γδ T cells was evaluated before or after IFN-α treatment in vitro.
Although γδT cells decreased in CHB patients during pegIFN-α therapy, their capacities to produce TNF-α and to express CD107a were enhanced. More effector γδT cells (CD27-CD45RA+) were found in the response group than in non-response group. Furthermore, IFN-α boosted the expression of Mx2 and cytokine genes in γδT cells from CHB patients in vitro.
IFN-α could enhance the cytokine production or cytotoxicity potential of γδT cells in vivo and in vitro. The enhanced function of γδT cells might contribute to the effect of IFN-α treatment.