Involvement of Th17 and Th1 Effector Responses in Patients with Hepatitis B

Ye, Yufu; Xie, Xiaojun; Yu, Jiwei; Zhou, Lin; Xie, Haiyang; Jiang, Guoping; Yu, Xiaobo; Zhang, Wenjin; Wu, Jian; Zheng, Shusen

doi:10.1007/s10875-010-9416-3

Cited by 76 publications

(65 citation statements)

References 38 publications

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“…This means that IL-17 did not contribute greatly to inflammation if released in an early innate environment, but it exerts more aggravating actions in the context of adaptive immune reactions. We also found that the patients with a higher HAI score had a greater proportion of Th17 cells than those patients with a lower HAI score, suggesting that Th17 cells might participate actively in the immunopathogenesis of paediatric patients with CHB, which is consistent with the observation in adult patients reported by Zhang et al [20] and Ye et al [12].…”

Section: Th17 Cells and Clinical Characterssupporting

confidence: 91%

“…It is well known that once the HBV infection is established, clearance of the virus is determined by the interactions between the virus and host factors [7,8]. A great deal of evidence has suggested that the cellular and humoral immune responses are essential for viral clearance, and that the non-HBVspecific immune response appears to be responsible for liver damage [9][10][11][12]. CD4 + T helper type (Th) cells have been described as playing a critical role in the pathogenesis of HBV infectious disease by providing help for cytotoxic T cells and producing cytokines [13].…”

Section: Introductionmentioning

confidence: 99%

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The correlation between T helper type 17 cells and clinical characters in Chinese paediatric patients with chronic hepatitis B

Zhu

Zhang

et al. 2013

Clinical and Experimental Immunology

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SummaryInterleukin (IL)-17-mediated immune response has been shown to play a critical role in inflammation-associated disease. However, its role in the pathogenesis of chronic hepatitis B virus (HBV) in paediatric patients remains unknown. We investigated the frequency of T helper type 17 (Th17) cells and evaluated the association between the Th17 and clinical characters in paediatric patients with chronic hepatitis B (CHB). The frequency of Th17 cells was detected by flow cytometry analyses from 65 paediatric patients with CHB and nine healthy controls. The degree of hepatic inflammation was graded using the histological activity index (HAI). Compared with healthy controls, the frequency of Th17 cells in peripheral blood was significantly higher in paediatric patients with CHB. The proportion of Th17 cells was higher in the patients with higher HAI score (G2-G3) compared to those subjects with lower HAI score (G0-G1), but the frequency of Th17 cells had no correlation with serum HBV DNA loads or alanine aminotransferase levels. Compared with the younger age group (age 1-6 years), Th17 cell frequency was higher in the older age group (age 7-18 years). Peripheral Th17 cell frequency is associated closely with inflammation activity of liver tissues in paediatric patients with CHB.

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Section: Th17 Cells and Clinical Characterssupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

The correlation between T helper type 17 cells and clinical characters in Chinese paediatric patients with chronic hepatitis B

Zhu

Zhang

et al. 2013

Clinical and Experimental Immunology

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“…The fact is that the functions of TH1 cells mainly protect against intracellular pathogens, while TH17 cells mainly protect against extracellular pathogens [38]. Inappropriate, excessive, and nonspecific Th17 and Th1 effector responses might be involved in persistent HBV replication and pathogenesis of HBV-associated liver inflammation [39,40]. The above results show that the neonatal innate immune defends against extracellular invading pathogens, but not intracellular pathogens such as HBV.…”

Section: Innate Immune Cells Employ Tlrs To Identify Hbv Invasionmentioning

confidence: 88%

Gut microbiota modulate the immune effect against hepatitis B virus infection

Huang

Wang

2015

Eur J Clin Microbiol Infect Dis

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The immunological mechanisms by which hepatitis B virus (HBV) initiates and maintains acute or chronic infection, even the formation of cirrhosis and hepatocellular carcinoma, are still undefined. An increasing number of studies have shown that intestinal flora regulate immune homeostasis, and, thus, protect the immunologic function against hepatitis virus infection. In this article, we discuss gut microbiota and its potential immune effects against HBV infection. It may provide a novel insight into the pathogenesis of HBV infection, as well as a potential therapeutic target to HBV-related disease.

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“…However, TNFα, IL-17 and T helper cell reactivity are positively correlated with the progression to chronic liver disease and acute-on-chronic liver failure in hepatitis B infection[39,64]. In addition, Zhou et al[70] (2012) observed a reduced frequency of the CD4 + IL-2 + IFNγ + TNF + population after resolution of hepatitis A, suggesting an increased risk of hepatitis relapse.…”

Section: Discussionmentioning

confidence: 99%

Changes in cellular proliferation and plasma products are associated with liver failure

Melgaço¹,

Soriani²,

Sucupira³

et al. 2016

WJH

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AIMTo study the differences in immune response and cytokine profile between acute liver failure and self-limited acute hepatitis.METHODSForty-six patients with self-limited acute hepatitis (AH), sixteen patients with acute liver failure (ALF), and twenty-two healthy subjects were involved in this study. The inflammatory and anti-inflammatory products in plasma samples were quantified using commercial enzyme-linked immunoassays and quantitative real-time PCR. The cellular immune responses were measured by proliferation assay using flow cytometry. The groups were divided into viral- and non-viral-induced self-limited AH and ALF. Thus, we worked with five groups: Hepatitis A virus (HAV)-induced self-limited acute hepatitis (HAV-AH), HAV-induced ALF (HAV-ALF), non-viral-induced self-limited acute hepatitis (non-viral AH), non-viral-induced acute liver failure (non-viral ALF), and healthy subjects (HC). Comparisons among HAV and non-viral-induced AH and ALF were performed.RESULTSThe levels of mitochondrial DNA (mtDNA) and the cytokines investigated [interleukin (IL)-6, IL-8, IL-10, interferon gamma, and tumor necrosis factor] were significantly increased in ALF patients, independently of etiology (P < 0.05). High plasma mtDNA and IL-10 were the best markers associated with ALF [mtDNA: OR = 320.5 (95%CI: 14.42-7123.33), P < 0.0001; and IL-10: OR = 18.8 (95%CI: 1.38-257.94), P = 0.028] and death [mtDNA: OR = 12.1 (95%CI: 2.57-57.07), P = 0.002; and IL-10: OR = 8.01 (95%CI: 1.26-50.97), P = 0.027]. In the cellular proliferation assay, NKbright, NKT and regulatory T cells (TReg) predominated in virus-specific stimulation in HAV-induced ALF patients with an anergic behavior in the cellular response to mitotic stimulation. Therefore, in non-viral-induced ALF, anergic behavior of activated T cells was not observed after mitotic stimulation, as expected and as described by the literature.CONCLUSIONmtDNA and IL-10 may be predictors of ALF and death. TReg cells are involved in immunological disturbance in HAV-induced ALF.

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Involvement of Th17 and Th1 Effector Responses in Patients with Hepatitis B

Cited by 76 publications

References 38 publications

The correlation between T helper type 17 cells and clinical characters in Chinese paediatric patients with chronic hepatitis B

The correlation between T helper type 17 cells and clinical characters in Chinese paediatric patients with chronic hepatitis B

Gut microbiota modulate the immune effect against hepatitis B virus infection

Changes in cellular proliferation and plasma products are associated with liver failure

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