Correlation of the expression of toll-like receptors in monocyte-derived dendritic cells with prognosis of chronic severe hepatitis B

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Abstract

This study aims to measure the expression of toll-like receptors (TLR) in monocyte-derived dendritic cells (MoDC) from chronic severe hepatitis B (CSHB), to assess the contribution of TLRs in CSHB. METHODS: Peripheral blood was collected from 40 CSHB patients, 30 chronic hepatitis B (CHB) patients, and 30 healthy individuals who served as healthy controls (HCs). Purified monocytes were isolated by a combination of Histopaque-1.077 and CD14 Microbeads. MoDCs were induced with granulocyte macrophage colony-stimulating factor and interleukin-4 for 6 days from CD14+ monocytes. The expression of TLRs in MoDC was measured using real-time PCR and flow cytometry. RESULTS: The expressions of TLR-1, -2, -7 were significantly higher in MoDC of CSHB than that of HCs, of which the level of TLR-3 was decreased. Particularly in CSHB patients, the TLR-3 expression was further decreased compared to CHB patients. In non-survival CSHB patients, TLR-3 level was significantly decreased, while TLR-2 expression was dramatically increased. Linear correlation analysis demonstrated significant correlations between TLR-3 level and disease severity markers (total bilirubin, prothrombin activity, creatinine, white blood cell count, and maximum volume of ascitic fluid) in individual CSHB patients. CONCLUSIONS: TLR-2 and TLR-3 may be involved in the pathogenesis of CSHB, and TLR-3 may influence the prognosis of CSHB. © 2011 The Authors. Journal of Digestive Diseases © 2011 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.

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Li, N., Chen, M. Q., Qian, Z. P., Zhu, M. Q., Li, Q., Zheng, J. M., … Shi, G. F. (2011). Correlation of the expression of toll-like receptors in monocyte-derived dendritic cells with prognosis of chronic severe hepatitis B. Journal of Digestive Diseases, 12(2), 117–124. https://doi.org/10.1111/j.1751-2980.2011.00486.x

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