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5. Defective circulating CD4+LAP+ regulatory T cells in patients with dilated cardiomyopathy

Author

Zhu, Zheng-Feng, primary, Tang, Ting-Ting, additional, Dong, Wen-Yong, additional, Li, Yuan-Yuan, additional, Xia, Ni, additional, Zhang, Wen-Cai, additional, Zhou, Su-Feng, additional, Yuan, Jing, additional, Liao, Meng-Yang, additional, Li, Jing-Jing, additional, Jiao, Jiao, additional, Nie, Shao-Fang, additional, Wang, Qing, additional, Tu, Xin, additional, Xu, Cheng-Qi, additional, Liao, Yu-Hua, additional, Shi, Guo-Ping, additional, and Cheng, Xiang, additional

Published
2015
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6. Impaired thymic export and increased apoptosis account for regulatory T cell defects in patients with non-ST segment elevation acute coronary syndrome.

Author

Zhang, Wen-cai, primary, Wang, Jun, additional, Shu, Yan-wen, additional, Tang, Ting-ting, additional, Zhu, Zheng-feng, additional, Xia, Ni, additional, Nie, Shao-fang, additional, Liu, Juan, additional, Zhou, Su-feng, additional, Li, Jing-jing, additional, Xiao, Hong, additional, Yuan, Jing, additional, Liao, Meng-yang, additional, Cheng, Long-xian, additional, Liao, Yu-hua, additional, and Cheng, Xiang, additional

Published
2013
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8. Impaired Thymic Export and Increased Apoptosis Account for Regulatory T Cell Defects in Patients with Non-ST Segment Elevation Acute Coronary Syndrome

Author

Zhang, Wen-cai, primary, Wang, Jun, additional, Shu, Yan-wen, additional, Tang, Ting-ting, additional, Zhu, Zheng-feng, additional, Xia, Ni, additional, Nie, Shao-fang, additional, Liu, Juan, additional, Zhou, Su-feng, additional, Li, Jing-jing, additional, Xiao, Hong, additional, Yuan, Jing, additional, Liao, Meng-yang, additional, Cheng, Long-xian, additional, Liao, Yu-hua, additional, and Cheng, Xiang, additional

Published
2012
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9. Correction: Impaired Thymic Export and Apoptosis Contribute to Regulatory T-Cell Defects in Patients with Chronic Heart Failure

Author

Tang, Ting-Ting, primary, Zhu, Zheng-Feng, additional, Wang, Jun, additional, Zhang, Wen-Cai, additional, Tu, Xin, additional, Xiao, Hong, additional, Du, Xin-Ling, additional, Xia, Jia-Hong, additional, Dong, Nian-Guo, additional, Su, Wei, additional, Xia, Ni, additional, Yan, Xin-Xin, additional, Nie, Shao-Fang, additional, Liu, Juan, additional, Zhou, Su-Feng, additional, Yao, Rui, additional, Xie, Jiang-Jiao, additional, Jevallee, Harish, additional, Wang, Xiang, additional, Liao, Meng-Yang, additional, Shi, Guo-Ping, additional, Fu, Michael, additional, Liao, Yu-Hua, additional, and Cheng, Xiang, additional

Published
2011
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10. Impaired Thymic Export and Apoptosis Contribute to Regulatory T-Cell Defects in Patients with Chronic Heart Failure

Author

Tang, Ting-Ting, primary, Zhu, Zheng-Feng, additional, Wang, Jun, additional, Zhang, Wen-Cai, additional, Tu, Xin, additional, Xiao, Hong, additional, Du, Xin-Ling, additional, Xia, Jia-Hong, additional, Dong, Nian-Guo, additional, Su, Wei, additional, Xia, Ni, additional, Yan, Xing-Xing, additional, Nie, Shao-Fang, additional, Liu, Juan, additional, Zhou, Su-Feng, additional, Yao, Rui, additional, Xie, Jiang-Jiao, additional, Jevallee, Harish, additional, Wang, Xiang, additional, Liao, Meng-Yang, additional, Shi, Guo-Ping, additional, Fu, Michael, additional, Liao, Yu-Hua, additional, and Cheng, Xiang, additional

Published
2011
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11. Atorvastatin upregulates regulatory T cells and reduces clinical disease activity in patients with rheumatoid arthritis

Author

Tang, Ting-Ting, primary, Song, You, additional, Ding, Ying-Jun, additional, Liao, Yu-Hua, additional, Yu, Xian, additional, Du, Rong, additional, Xiao, Hong, additional, Yuan, Jing, additional, Zhou, Zi-Hua, additional, Liao, Meng-Yang, additional, Yao, Rui, additional, Jevallee, Harish, additional, Shi, Guo-Ping, additional, and Cheng, Xiang, additional

Published
2011
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13. Defective circulating CD4+LAP+regulatory T cells in patients with dilated cardiomyopathy

Author

Zhu, Zheng‐Feng, Tang, Ting‐Ting, Dong, Wen‐Yong, Li, Yuan‐Yuan, Xia, Ni, Zhang, Wen‐Cai, Zhou, Su‐Feng, Yuan, Jing, Liao, Meng‐Yang, Li, Jing‐Jing, Jiao, Jiao, Nie, Shao‐Fang, Wang, Qing, Tu, Xin, Xu, Cheng‐Qi, Liao, Yu‐Hua, Shi, Guo‐Ping, and Cheng, Xiang

Abstract

The decreased number and dysfunctional of CD4+LAP+Tregsmay be an underlying mechanism of immune activation inDCM patients. There has been increasing evidence that chronic immune activation plays critical roles in the pathogenesis of DCM. CD4+LAP+Tregsare a newly identified T cell subset with suppressive function on the immune response. This study was designed to investigate whether the circulating frequency and function of CD4+LAP+Tregswould be impaired in patients with DCM. The results demonstrated that DCM patients had a significantly lower frequency of circulating CD4+LAP+Tregscompared with control donors. CD4+LAP+Tregsfrom DCM patients showed compromised function to suppress proliferation of CD4+LAP−CD25int/lowT cells and proliferation and IgG production of B cells. Moreover, B cell proliferation and IgG subset production could be directly suppressed by CD4+LAP+Tregs. TGF‐βand contact‐dependent mechanisms were involved in CD4+LAP+Treg‐mediated suppression. Correlation analysis suggested that CD4+LAP+Tregfrequency was positively correlated with LVEF and negatively correlated with serum IgG3 and NT‐proBNP concentration in patients with DCM. Our results are the first to demonstrate that the frequencies of CD4+LAP+Tregsin patients with DCM are reduced and that their suppressive function is compromised. Defective CD4+LAP+Tregsmay be an underlying mechanism of immune activation in DCM patients.

Published
2015
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14. The Th17/Treg functional imbalance during atherogenesis in ApoE−/− mice

Author

Xie, Jiang-jiao, Wang, Jun, Tang, Ting-ting, Chen, Jian, Gao, Xing-li, Yuan, Jing, Zhou, Zi-hua, Liao, Meng-yang, Yao, Rui, Yu, Xian, Wang, Dan, Cheng, Yan, Liao, Yu-hua, and Cheng, Xiang

Subjects
*INFLAMMATION, *LYMPHOCYTES, *LABORATORY mice, *AUTOIMMUNITY, *TRANSFORMING growth factors-beta, *GENE expression, *CYTOKINES, *TRANSCRIPTION factors
Abstract

Abstract: Objective: Atherosclerosis is a chronic inflammatory disease regulated by T lymphocyte subsets. Recently, CD4+ CD25+ Foxp3+ regulatory T (Treg) cells and Th17 cells have been described as two distinct subsets and have the opposite effects on autoimmunity. Clinical observation has revealed that the Th17/Treg imbalance exists in patients with acute coronary syndrome. We investigated whether the Th17/Treg functional imbalance existed during atherogenesis in ApoE−/− mice. Methods and results: Th17/Treg functions at different levels including cell frequencies, related cytokine secretion and key transcription factors were investigated comparatively between ApoE−/− mice and their age-matched C57BL/6J mice. The results demonstrated that ApoE−/− mice revealed significantly increased secretion of Th17 related cytokines (IL-17 and IL-6) and expression of transcription factor (RORγt) levels and obviously decreased number in Treg cells, secretion of Treg related cytokines (TGF-β1) and expression of transcription factor (Foxp3) levels as compared with age-matched C57BL/6J mice. Th17 related mediators reached their maximum expression values at the early stage (8–16weeks of age) in ApoE−/− mice, and then followed by continuous depression of their expression levels. Meanwhile, the expression of Treg related mediators was much lower in ApoE−/− mice than in their age-matched wild-type littermates. Conclusions: Th17/Treg functional imbalance exists during atherogenesis in ApoE−/− mice, suggesting a potential role of Th17/Treg imbalance in the formation and progression of atherosclerosis. [Copyright &y& Elsevier]

Published
2010
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15. MicroRNA-155 induces differentiation of RAW264.7 cells into dendritic-like cells.

Author

Ma YL, Ma ZJ, Wang M, Liao MY, Yao R, and Liao YH

Subjects
Animals, CD36 Antigens metabolism, Cell Shape, Cytokines metabolism, Dendritic Cells drug effects, Dendritic Cells immunology, Inflammation Mediators metabolism, Lipopolysaccharides pharmacology, Lipoproteins, LDL pharmacology, Macrophages drug effects, Macrophages immunology, Mice, MicroRNAs genetics, Phenotype, RAW 264.7 Cells, Time Factors, Up-Regulation, Cell Transdifferentiation, Dendritic Cells metabolism, Macrophages metabolism, MicroRNAs metabolism
Abstract

MicroRNA (miRNA, miR)-155 is the most promising pro-inflammatory miRNA molecule. Lipopolysaccharide (LPS) and oxidized low-density lipoprotein (oxLDL) are the most well-known foreign antigens, initiating immune responses against infection and the development of atherosclerosis (AS), respectively. To explore whether miR-155 is involved in regulating LPS- and oxLDL-initiated inflammations, we investigated the level of miR-155 in both LPS- and oxLDL-treated RAW264.7 cells, assessed whether miR-155 induce morphologic changes of the cells and how did it regulate the production of surface markers and cytokines. The results showed that the level of miR-155 was significantly increased by LPS and was modestly increased by oxLDL. Moreover, RAW264.7 cells displayed morphological transformations from macrophage-like cells into DC-like cells when miR-155 was over-expressed. Furthermore, the gain- and loss-of-function studies demonstrated that miR-155 induced the expression of the surface markers (including MHC-II, MHC-I, CD86, and CD83) and pro-inflammatory cytokines (including interleukin (IL)-12, IL-6, and IL-1b) in both LPS- and oxLDL-treated RAW264.7 cells. Additionally, miR-155 induced the expression of CD36 in oxLDL-treated RAW264.7 cells. In conclusion, up-regulated miR-155 is able to induce morphological and phenotypic changes, and the expression of pro-inflammatory cytokines in both LPS- and oxLDL-treated RAW264.7 cells. Therefore, our study suggests that miR-155 is one important regulator involved in enhancing both LPS- and oxLDL-initiated inflammations, which is critical for the progression of immune responses as well as for the development of AS.

Published
2015

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