Severe dendritic cell perturbation is actively involved in the pathogenesis of acute-on-chronic hepatitis B liver failure

Zhang, Zheng; Zou, Zhengsheng; Fu, Junliang; Cai, Lun; Jin, Lei; Liu, Yongjun; Wang, Fusheng

doi:10.1016/j.jhep.2008.05.017

Cited by 94 publications

(92 citation statements)

References 40 publications

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“…Previous data from our laboratory have indicated that both mDCs and pDCs infiltrate extensively the liver of ACLF patients and have expressed mature phenotypes. 8,14 Therefore, this DC migration from the blood to the liver may lead to the decreased DC numbers found in the blood, while infiltrated DCs in liver may be involved in the pathogenesis of ACLF. This study found that the decreased numbers of mDC at baseline was associated with a high mortality of ACLF patients and further indicated that the mDC numbers of the host may determine the outcome of ACLF patients.…”

Section: Discussionmentioning

confidence: 99%

“…7,8,14 Two distinct circulating dendritic cell (DC) subsets, myeloid and plasmacytoid DCs (mDCs and pDCs), have been identified in humans based on phenotypic and functional characterizations. 15,16 In general, human mDCs are well equipped to induce type 1 T helper cell polarization via the production of interleukin-12 (IL-12) or tumor-necrosis factor-a, which plays a crucial role in the development of liver damage.…”

Section: 2mentioning

confidence: 99%

“…Recent studies have demonstrated the functional impairment of mDCs and pDCs in patients with chronic HBV infection. [17][18][19] Notably, these dendritic cells accumulate mostly in the liver of ACLF patients; 7,8,14 however, any correlation between the DCs and corticosteroid efficacy is unknown.…”

Section: 2mentioning

confidence: 99%

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Improved survival ratios correlate with myeloid dendritic cell restoration in acute-on-chronic liver failure patients receiving methylprednisolone therapy

Zhao

Zhang

et al. 2012

Cell Mol Immunol

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Acute-on-chronic liver failure (ACLF) is a severe life-threatening complication. Liver transplantation is the only available therapeutic option; however, several limitations have restricted its use in patients. The use of corticosteroids as an optional therapy for ACLF has received a great deal of interest. The rationale behind its use is the possible role of the immune system in initiating and perpetuating hepatic damage. In order to assess the relationship between myeloid dendritic cells (mDCs) and the efficacy of methylprednisolone (MP) treatment for hepatitis B virus (HBV)-associated ACLF patients, we recruited 30 HBV-associated ACLF patients who had received MP treatment at 10-day intervals; 26 patients received conservative medical (CM) management as a control. The functionality of DC subsets was lower in these ACLF patients compared with healthy subjects. In addition, compared with survivors, dead/transplanted patients had lower functional mDC in both groups. Furthermore, a decreased numbers of mDC at baseline was associated with high mortality of ACLF patients. Importantly, MP treatment resulted in a significant decrease in 28-day mortality, and all MP patients exhibited an initial rapid decrease in circulating mDC numbers within 10 days of MP treatment. Subsequently, MP survivors displayed a continuous increase in mDC numbers accompanied by a decrease in total bilirubin levels by more than 30%. However, MP dead/ transplanted patients lacked these sequential responses compared with survivors. This evidence suggests strongly that the higher mDC numbers at baseline and the recovery of mDC number at the end of treatment may represent a prognostic marker for favorable response to corticosteroid treatment in ACLF patients.

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Section: Discussionmentioning

confidence: 99%

Section: 2mentioning

confidence: 99%

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Improved survival ratios correlate with myeloid dendritic cell restoration in acute-on-chronic liver failure patients receiving methylprednisolone therapy

Zhao

Zhang

et al. 2012

Cell Mol Immunol

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“…T cells. When intrahepatic mononuclear cells obtained from HBV-infected patients were cultured in vitro, blockade of plasmacytoid DC (pDC)-derived IFN-a downregulated the amounts of interleukin (IL)-12 and TNF-a released from adjacent cells [14], suggesting that liver pDCs play a pivotal role in regulating immune responses in situ. We have recently shown that pDCs are a key player in the inhibition of HBV replication by producing IFN-a upon primary HBV infection either directly or indirectly through their activation of NK cells [15].…”

Section: Innate Immunity In Hbv Infection: the Role Of Nk Cells And Dcsmentioning

confidence: 99%

“…However, several reports are available on functional alterations of DC subsets in HBV infection [39], including a report of reduced pDC frequency and reduced expression of TLR9 by pDCs [40]. Liver-infiltrating pDCs are more vulnerable to HBV than their peripheral counterparts; liver pDCs have been reported to be significantly reduced and disabled in non-survivors of acute-on-chronic hepatitis B compared to those in survivors [14]. The ability of pDCs to produce IFN-a is impaired specifically in response to TLR9 but not to TLR7 agonists [41].…”

Section: Nk Cells and Dcs In Chronic Hbv Infectionmentioning

confidence: 99%

Host–virus interactions in hepatitis B and hepatitis C infection

Yoshio

Kanto

2016

J Gastroenterol

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Hepatitis B virus (HBV) and hepatitis C virus (HCV) are among the most endemic pathogens worldwide, with more than 500 million people globally currently infected with these viruses. These pathogens can cause acute and chronic hepatitis that progress to liver cirrhosis or hepatocellular carcinoma. Both viruses utilize multifaceted strategies to evade the host surveillance system and fall below the immunological radar. HBV has developed specific strategies to evade recognition by the innate immune system and is acknowledged to be a stealth virus. However, extensive research has revealed that HBV is recognized by dendritic cells (DCs) and natural killer (NK) cells. Indoleamine-2, 3-dioxygenase is an enforcer of sequential immune reactions in acute hepatitis B, and this molecule has been shown to be induced by the interaction of HBV-infected hepatocytes, DCs, and NK cells. The interleukin-28B genotype has been reported to influence HCV eradication either therapeutically or spontaneously, but the biological function of its gene product, a type-III interferon (IFN-k3), remains to be elucidated. Human BDCA3 ? DCs have also been shown to be a potent producer of IFN-k3 in HCV infection, suggesting the possibility that BDCA3 ? DCs could play a key role in developing therapeutic HCV vaccine. Here we review the current state of research on immune responses against HBV and HCV infection, with a specific focus on innate immunity. A comprehensive study based on clinical samples is urgently needed to improve our understanding of the immune mechanisms associated with viral control and thus to develop novel immune modulatory therapies to cure chronic HBV and HCV infection.

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Optimization of the properties of chitosan lactate/hyaluronan film

Kukolíková

Bakoš

Alexy

et al. 2006

J of Applied Polymer Sci

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Polyelectrolyte complexes represent attractive class of polymer-based materials, finding an irreplaceable role in biomaterial preparation for tissue engineering or drug delivery beads. Mechanical properties, physical properties, and enzymatic degradation of the film prepared from chitosan lactate/hyaluronan polyelectrolyte complex, crosslinked with starch dialdehyde derivatives, were studied to optimize its composition. This work represents an example demonstrating how a minor modification of the modified complex composition changes final properties of the prepared film and emphasizes enormous variations in complex formation by crosslinking. To obtain sufficiently useful information, experimental design was employed.

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Severe dendritic cell perturbation is actively involved in the pathogenesis of acute-on-chronic hepatitis B liver failure

Cited by 94 publications

References 40 publications

Improved survival ratios correlate with myeloid dendritic cell restoration in acute-on-chronic liver failure patients receiving methylprednisolone therapy

Improved survival ratios correlate with myeloid dendritic cell restoration in acute-on-chronic liver failure patients receiving methylprednisolone therapy

Host–virus interactions in hepatitis B and hepatitis C infection

Optimization of the properties of chitosan lactate/hyaluronan film

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