Pattern recognition receptor responses in children with chronic hepatitis B virus infection

Heiberg, Ida Louise; Winther, Thilde Nordmann; Paludan, Søren R.; Høgh, Birthe

doi:10.1016/j.jcv.2012.04.013

Cited by 12 publications

(9 citation statements)

References 27 publications

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“…However, analysis of TLR expression in PBMCs from patients with varying phases of clinical chronic HBV infection found that the expression of TLR3 (in addition to other TLRs) was enhanced in active-stage CHB and CHB-related liver failure [173]. Furthermore, in PBMCs from children with CHB, TLR3 and other TLRs were found to induce inflammatory cytokines and chemokines to a significantly higher level compared with healthy children [174]. Together, despite some contradictory findings, these findings suggest that TLR3/TRIF-mediated signaling and inflammation play an important role in HBV infection and that dysregulated or inadequate TLR3/TRIF immune responses may predispose patients to detrimental outcomes.…”

Section: Trif-dependent Antiviral Responsesmentioning

confidence: 99%

TRIF-dependent TLR signaling, its functions in host defense and inflammation, and its potential as a therapeutic target

Ullah

Sweet

Mansell

et al. 2016

Journal of Leukocyte Biology

167

108

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Toll/IL-1R domain-containing adaptor-inducing IFN-β (TRIF)-dependent signaling is required for TLR-mediated production of type-I IFN and several other proinflammatory mediators. Various pathogens target the signaling molecules and transcriptional regulators acting in the TRIF pathway, thus demonstrating the importance of this pathway in host defense. Indeed, the TRIF pathway contributes to control of both viral and bacterial pathogens through promotion of inflammatory mediators and activation of antimicrobial responses. TRIF signaling also has both protective and pathologic roles in several chronic inflammatory disease conditions, as well as an essential function in wound-repair processes. Here, we review our current understanding of the regulatory mechanisms that control TRIF-dependent TLR signaling, the role of the TRIF pathway in different infectious and noninfectious pathologic states, and the potential for manipulating TRIF-dependent TLR signaling for therapeutic benefit.

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Section: Trif-dependent Antiviral Responsesmentioning

confidence: 99%

TRIF-dependent TLR signaling, its functions in host defense and inflammation, and its potential as a therapeutic target

Ullah

Sweet

Mansell

et al. 2016

Journal of Leukocyte Biology

167

108

View full text Add to dashboard Cite

show abstract

“…A ≥5% increase in [5, [18][19][20][21]. Furthermore, Heiberg et al [22] describe reduced interferon-a production after TLR3 ligand stimulation in CHB children. Wu et al [23] provide evidence that HBV suppresses TLR-induced antiviral activity in the liver, and studies by Yu et al [24] reveal that HBV polymerase is the potent inhibitor of TLR3mediated interferon-b induction.…”

Section: Tlr3 Expression On Pbmcs Of Chb Patients During Pegylated Interferon or Entecavir Therapymentioning

confidence: 99%

Reduced Toll-Like Receptor 3 Expression in Chronic Hepatitis B Patients and Its Restoration by Interferon Therapy

et al. 2013

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“…The interaction of TLRs in different models of HBV infection is shown in Figure 1 ( Figure 1 A–F), which suggests the crucial role of TLR response in inhibiting HBV infection. In this regard, we also have shown the association of TLRs with other molecules, including IRAK4, TRAF3, and IRF7 in the induction of IL-6, CCL3, and CXCL10 [ 36 , 49 , 74 ] ( Figure 1 G). Therefore, a proper understanding of TLR responses in HBV infection is critical for successful therapeutic or preventive interventions.…”

Section: Tlr Response To Hbv Infectionmentioning

confidence: 75%

“…The cells also showed an impaired cytokine response after stimulation with TLR2 and TLR4 agonists, which correlated with the plasma HBsAg level of the patients [ 48 ], suggesting a possible interaction between HBsAg and TLR signaling. Another study showed that after stimulation with ligands for TLR2, TLR3, and TLR9 on PBMCs obtained from children with chronic HBV infection, there was an increase in production of IL-6, CCL3, and CXCL10 [ 49 ], indicating the induction of TLR-mediated inflammatory response. However, on stimulation with ligands for TLR2, TLR3, and TLR4, the PBMCs from children with CHB showed a significantly lower IFN-α production than in those from healthy children [ 49 ], suggesting a suppressed IFN response.…”

Section: Tlr Response To Hbv Infectionmentioning

confidence: 99%

“…Another study showed that after stimulation with ligands for TLR2, TLR3, and TLR9 on PBMCs obtained from children with chronic HBV infection, there was an increase in production of IL-6, CCL3, and CXCL10 [ 49 ], indicating the induction of TLR-mediated inflammatory response. However, on stimulation with ligands for TLR2, TLR3, and TLR4, the PBMCs from children with CHB showed a significantly lower IFN-α production than in those from healthy children [ 49 ], suggesting a suppressed IFN response. A significantly decreased expression of TLR signaling molecules, including IRAK4, TRAF3, and IRF7, was found in PBMCs of patients with CHB, as compared to that in those of healthy controls [ 50 ], suggesting an impaired immune response in chronic HBV infection.…”

Section: Tlr Response To Hbv Infectionmentioning

confidence: 99%

See 1 more Smart Citation

Toll-Like Receptor Response to Hepatitis B Virus Infection and Potential of TLR Agonists as Immunomodulators for Treating Chronic Hepatitis B: An Overview

Kayesh

Kohara

Tsukiyama-Kohara

2021

IJMS

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Chronic hepatitis B virus (HBV) infection remains a major global health problem. The immunopathology of the disease, especially the interplay between HBV and host innate immunity, is poorly understood. Moreover, inconsistent literature on HBV and host innate immunity has led to controversies. However, recently, there has been an increase in the number of studies that have highlighted the link between innate immune responses, including Toll-like receptors (TLRs), and chronic HBV infection. TLRs are the key sensing molecules that detect pathogen-associated molecular patterns and regulate the induction of pro- and anti-inflammatory cytokines, thereby shaping the adaptive immunity. The suppression of TLR response has been reported in patients with chronic hepatitis B (CHB), as well as in other models, including tree shrews, suggesting an association of TLR response in HBV chronicity. Additionally, TLR agonists have been reported to improve the host innate immune response against HBV infection, highlighting the potential of these agonists as immunomodulators for enhancing CHB treatment. In this study, we discuss the current understanding of host innate immune responses during HBV infection, particularly focusing on the TLR response and TLR agonists as immunomodulators.

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Pattern recognition receptor responses in children with chronic hepatitis B virus infection

Cited by 12 publications

References 27 publications

TRIF-dependent TLR signaling, its functions in host defense and inflammation, and its potential as a therapeutic target

TRIF-dependent TLR signaling, its functions in host defense and inflammation, and its potential as a therapeutic target

Reduced Toll-Like Receptor 3 Expression in Chronic Hepatitis B Patients and Its Restoration by Interferon Therapy

Toll-Like Receptor Response to Hepatitis B Virus Infection and Potential of TLR Agonists as Immunomodulators for Treating Chronic Hepatitis B: An Overview

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