Evidence map›Paper›PMID 25661729›Full record

ArticleCellular & molecular immunology2015

Tumor necrosis factor-alpha blockage therapy impairs hepatitis B viral clearance and enhances T-cell exhaustion in a mouse model.

I-Tsu Chyuan, Hwei-Fang Tsai, Horng-Tay Tzeng, Chi-Chang Sung, Chien-Sheng Wu, Pei-Jer Chen, Ping-Ning Hsu

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular & molecular immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 30 citations in OpenAlex.

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  12. γδ T cells in liver diseases.Frontiers of medicine · 2018
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

I-Tsu Chyuan1] Department of Internal Medicine, Cathay General Hospital, Taipei, Taiwan, China [2] Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan, China.
Hwei-Fang Tsai1] Department of Internal Medicine, Taipei Medical University Shuang Ho Hospital, Taipei, Taiwan, China [2] Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan, China.
Horng-Tay TzengGraduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan, China.
Chi-Chang SungGraduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan, China.
Chien-Sheng WuDepartment of Internal Medicine, Far Eastern Memorial Hospital, New Taipei City, Taiwan, China.
Pei-Jer ChenGraduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan, China.
Ping-Ning Hsu1] Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan, China [2] Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan, China.
National Taiwan University · TWCathay General Hospital · TWFar Eastern Memorial Hospital · TWTaipei Medical University-Shuang Ho Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) reactivation and recurrence are common in patients undergoing immunosuppression therapy. Tumor necrosis factor (TNF) blockage therapy is effective for the treatment of many autoimmune inflammatory diseases. However, the role of TNF-α blockage therapy in the innate and adaptive immune responses against HBV is still not clear. A detailed analysis of HBV infection under TNF-α blockage therapy is essential for the prophylaxis and therapy for HBV reactivation and recurrence. In this study, HBV clearance and T-cell responses were analyzed in a HBV-transfected mouse model under anti-TNF blockage therapy. Our results demonstrated that under TNF-α blockage therapy, HBV viral clearance was impaired with persistent elevated HBV viral load in a dose- and temporal-dependent manner. The impairment of HBV clearance under anti-TNF-α blockage therapy occurred at early time points after HBV infection. In addition, TNF-α blockade maintained a higher serum HBV viral load and increased the number of intrahepatic programmed cell death (PD)-1(high)CD127(low) exhausted T cells. Furthermore, TNF-α blockade abolished Toll-like receptor 9 (TLR9) ligand-induced facilitation of HBV viral clearance. Taken together, TNF-α blockade impairs HBV clearance and enhances viral load, and these effects depend on early administration after HBV infection. Our results here demonstrate that early TNF-α blockade reduces viral clearance and persistently maintains elevated HBV viral load in a mouse model, suggesting that HBV may reactivate during therapy with TNF-α-blocking agents.

Indexed as

ImmunotherapyAnimalsAntibodies, BlockingCell SurvivalDisease Models, AnimalHepacivirusHepatitis BHumansImmunosuppression TherapyInterleukin-7 Receptor alpha SubunitMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutProgrammed Cell Death 1 ReceptorAntibodies, BlockingInterleukin-7 Receptor alpha SubunitPdcd1 protein, mouseProgrammed Cell Death 1 ReceptorTlr9 protein, mouseToll-Like Receptor 9Tumor Necrosis Factor-alpha

Identifiers

PMID25661729
PMCPMC4654324
OpenAlexW2016460303

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.