Evidence map›Paper›PMID 29271379›Full record

ArticleChinese medical journal2018

Plasmacytoid Dendritic Cell Function and Cytokine Network Profiles in Patients with Acute or Chronic Hepatitis B Virus Infection.

Ming-Hui Li, Lu Zhang, Dan Zhang, Wei-Hua Cao, Tian-Lin Qi, Hong-Xiao Hao, Xing-Yue Wang, Chong-Ping Ran, Xiao-Jing Qu, Shun-Ai Liu and 10 more

Open access · goldAbstract read
In one paragraph

Article in Chinese medical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  5. Observational
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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

20 authors at 2 institutions in 1 country.

Ming-Hui LiLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Lu ZhangLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Dan ZhangLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Wei-Hua CaoLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Tian-Lin QiLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Hong-Xiao HaoLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Xing-Yue WangLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Chong-Ping RanLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Xiao-Jing QuLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Shun-Ai LiuInstitute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Yao LuLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Ge ShenLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Shu-Ling WuLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Min ChangLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Ru-Yu LiuLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Lei-Ping HuLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Wen-Hao HuaClinical Test Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Gang WanLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Jun ChengInstitute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Yao XieLiver Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China.
Beijing Ditan Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlasmacytoid dendritic cells (pDCs) and cytokines play an important role in occurrence and recovery of hepatitis B virus (HBV) infection. The aim of this study was to explore the frequency and function of pDC and serum cytokine network profiles in patients with acute or chronic HBV infection.

methodsThe healthy individuals (HI group), hepatitis B envelope antigen (HBeAg)-positive chronic HBV patients in immune tolerance (IT) phase (IT group), HBeAg-positive chronic HBV patients (CHB group), and acute HBV patients (AHB group) were enrolled in this study. The frequency of cluster of differentiation antigen 86 (CD86) + pDC and the counts of CD86 molecular expressed on surface of pDC were tested by flow cytometer. The quantitative determinations of cytokines, including Fms-like tyrosine kinase 3 ligand (Flt-3L), interferon (IFN)-α2, IFN-γ, interleukin (IL)-17A, IL-6, IL-10, transforming growth factor (TGF)-β1 and TGF-β2, were performed using Luminex multiplex technology.

resultsIn this study, there were 13 patients in HI group, 30 in IT group, 50 in CHB group, and 32 in AHB group. Compared with HI group, HBV infected group (including all patients in IT, CHB and AHB groups) had significantly higher counts of CD86 molecular expressed on the surface of pDC (4596.5 ± 896.5 vs. 7097.7 ± 3124.6; P < 0.001). The counts of CD86 molecular expressed on the surface of pDC in CHB group (7739.2 ± 4125.4) was significantly higher than that of IT group (6393.4 ± 1653.6, P = 0.043). Compared with IT group, the profile of cytokines of Flt-3L, IFN-γ, and IL-17A was decreased, IFN-α2 was significantly increased (P = 0.012) in CHB group. The contents of IL-10, TGF-β1, and TGF-β2 in AHB group were significantly increased compared with IT and CHB groups (all P < 0.05).

conclusionsThis study demonstrated that the function of pDC was unaffected in HBV infection. The enhanced function of pDC and IFN-α2 might involve triggering the immune response from IT to hepatitis active phase in HBV infection. Acute patients mainly presented as down-regulation of the immune response by enhanced IL-10 and TGF-β.

Indexed as

Acute DiseaseAdultAlbuminsBilirubinCreatinineCytokinesDendritic CellsFemaleHepatitis BHepatitis B, ChronicHepatitis B Surface AntigensHumansImmune ToleranceMaleMiddle AgedTransaminasesAlbuminsBilirubinCreatinineCytokinesHepatitis B Surface AntigensTransaminases

Identifiers

PMID29271379
PMCPMC5754957
OpenAlexW2781925351

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.