Evidence map›Paper›PMID 27174425›Full record

Trial reportScientific reports2016

CD3(bright)CD56(+) T cells associate with pegylated interferon-alpha treatment nonresponse in chronic hepatitis B patients.

Chuang Guo, Xiaokun Shen, Binqing Fu, Yanyan Liu, Yongyan Chen, Fang Ni, Ying Ye, Rui Sun, Jiabin Li, Zhigang Tian and 1 more

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. NKp30Scientific reports · 2016
    Trial
  2. Article
  3. Deficient IL-2 Produced by Activated CD56Frontiers in immunology · 2019
    Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Chuang GuoInstitute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei 230027, People's Republic of China.
Xiaokun ShenInstitute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei 230027, People's Republic of China.
Binqing FuInstitute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei 230027, People's Republic of China.
Yanyan LiuDepartment of Infectious Diseases, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China.
Yongyan ChenInstitute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei 230027, People's Republic of China.
Fang NiInstitute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei 230027, People's Republic of China.
Ying YeDepartment of Infectious Diseases, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China.
Rui SunInstitute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei 230027, People's Republic of China.
Jiabin LiDepartment of Infectious Diseases, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China.
Zhigang TianInstitute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei 230027, People's Republic of China.
Haiming WeiInstitute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei 230027, People's Republic of China.
University of Science and Technology of China · CNAnhui Medical University · CNHefei National Center for Physical Sciences at Nanoscale · CNFirst Affiliated Hospital of Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic hepatitis B (CHB) infection is a serious and prevalent health concern worldwide, and the development of effective drugs and strategies to combat this disease is urgently needed. Currently, pegylated interferon-alpha (peg-IFNα) and nucleoside/nucleotide analogues (NA) are the most commonly prescribed treatments. However, sustained response rates in patients remain low, and the reasons are not well understood. Here, we observed that CHB patients preferentially harbored CD3(bright)CD56(+) T cells, a newly identified CD56(+) T cell population. Patients with this unique T cell population exhibited relatively poor responses to peg-IFNα treatment. CD3(bright)CD56(+) T cells expressed remarkably high levels of the inhibitory molecule NKG2A as well as low levels of CD8. Even if patients were systematically treated with peg-IFNα, CD3(bright)CD56(+) T cells remained in an inhibitory state throughout treatment and exhibited suppressed antiviral function. Furthermore, peg-IFNα treatment rapidly increased inhibitory TIM-3 expression on CD3(bright)CD56(+) T cells, which negatively correlated with IFNγ production and might have led to their dysfunction. This study identified a novel CD3(bright)CD56(+) T cell population preferentially shown in CHB patients, and indicated that the presence of CD3(bright)CD56(+) T cells in CHB patients may be useful as a new indicator associated with poor therapeutic responses to peg-IFNα treatment.

Indexed as

AdultAntiviral AgentsCD3 ComplexCD56 AntigenCD8 AntigensFemaleHepatitis B, ChronicHepatitis B virusHep G2 CellsHumansInterferon-alphaMaleNK Cell Lectin-Like Receptor Subfamily COutcome Assessment, Health CarePolyethylene GlycolsT-LymphocytesAntiviral AgentsCD3 ComplexCD56 AntigenCD8 AntigensInterferon-alphaNK Cell Lectin-Like Receptor Subfamily CPolyethylene Glycols

Identifiers

PMID27174425
PMCPMC4865958
OpenAlexW2380491159

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.