Evidence map›Paper›PMID 30695096›Full record

ArticleJournal of gastroenterology and hepatology2019

The balance of type 1 and type 2 immune responses in the contexts of hepatitis B infection and hepatitis D infection.

Elizabeth C Townsend, Grace Y Zhang, Rabab Ali, Marian Firke, Mi Sun Moon, Ma Ai Thanda Han, Benjamin Fram, Jeffrey S Glenn, David E Kleiner, Christopher Koh and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of gastroenterology and hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Hepatitis Delta Virus and Hepatocellular Carcinoma.Pathogens (Basel, Switzerland) · 2024
    Review
  6. CCL13 and human diseases.Frontiers in immunology · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Human hepatitis D virus-specific T cell epitopes.JHEP reports : innovation in hepatology · 2021
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
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.

Elizabeth C TownsendLiver Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, Bethesda, Maryland, USA.ORCID https://orcid.org/0000-0003-3102-8033
Grace Y ZhangLiver Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, Bethesda, Maryland, USA.
Rabab AliLiver Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, Bethesda, Maryland, USA.
Marian FirkeLiver Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, Bethesda, Maryland, USA.
Mi Sun MoonLiver Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, Bethesda, Maryland, USA.
Ma Ai Thanda HanLiver Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, Bethesda, Maryland, USA.
Benjamin FramDepartment of Medicine, Stanford University, Stanford, California, USA.
Jeffrey S GlennDepartment of Medicine, Stanford University, Stanford, California, USA.
David E KleinerLaboratory of Pathology, National Cancer Institute, Bethesda, Maryland, USA.
Christopher KohLiver Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, Bethesda, Maryland, USA.
Theo HellerLiver Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, Bethesda, Maryland, USA.
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · USStanford University · USUnited States Department of Veterans Affairs · US

Funding

Postmortem PathologyZICBC010685 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KLEINER, DAVID ERWIN · 2009 to 2025
$14.3M
Investigation of management and disease manifestations of viral hepatitisZIADK054514 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HELLER, THEO · 2009 to 2025
$12.9M
Management and Treatment of Chronic Delta Hepatitis Infection and other Liver DiseasesZIADK075150 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOH, CHRISTOPHER · 2019 to 2025
$2.8M
Postmortem PathologyZ01BC010685 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KLEINER, DAVID E · 2005 to 2008
$913k
Intramural National Institutes of Health FundingIntramural NIH HHS Z01 BC010685Intramural NIH HHS ZIA DK054514
6 · The paper itself

Abstract

BACKGROUND AND

aimHepatitis delta virus (HDV) infection is the most rapidly progressive chronic viral hepatitis. Little is understood about the immune responses to HDV. This study aims to characterize the systemic immune environments of hepatitis B virus (HBV) and HDV patients at various disease stages.

methodsA total of 129 subjects were evaluated: 53 HBV, 43 HDV, and 33 healthy controls. HBV and HDV subjects were categorized by aspartate aminotransferase to platelet ratio index (APRI) into mild (APRI < 0.5), moderate, and severe (APRI > 1.0). Serum cytokines and immune markers were assessed at a single treatment-naïve time-point.

resultsType 1 cytokines are elevated in both HBV and HDV. Both groups show higher tumor necrosis factor-α (TNF-α), interleukin (IL)-12p40, and C-X-C motif chemokine ligand 9 when compared with controls (all P < 0.05). However, only HBV group displayed elevated γ-interferon compared with controls. Type 2 cytokines are elevated in HBV. HBV group shows higher IL-4, IL-13, and C-C motif chemokine ligand (CCL) 26 compared with healthy controls and HDV. Chemokines CCL2 and CCL13 are lower in HDV. When assessing ratios, HDV displays higher γ-interferon/IL-4, TNF-α/IL-4, and TNF-α/IL-13 ratios than HBV and controls.

conclusionHepatitis B virus and HDV subjects show similarly elevated type 1 cytokines. HDV subjects display relatively lower type 2 cytokines. These differences in the systemic immune environments, particularly the predominance of type 1 responses, may contribute to the comparatively rapid progression of HDV disease. Characterization of the imbalance in type 1 and type 2 immunity unique HDV has the potential to provide immunological insights for designing therapeutic targets in HDV-associated disease progression.

Indexed as

AdultAgedChemokine CCL2Chemokines, CXCCytokinesDisease ProgressionFemaleHepatitis BHepatitis B virusHepatitis DHepatitis Delta VirusHumansInterferon-gammaInterleukin-12Interleukin-13Interleukin-4Chemokine CCL2Chemokines, CXCCytokinesInterferon-gammaInterleukin-12Interleukin-13Interleukin-4Tumor Necrosis Factor-alphacytokineshepatitis B virus (HBV)hepatitis delta virus (HDV)immune system

Identifiers

PMID30695096
PMCPMC8237314
OpenAlexW2914929233

What OpenQuestion holds

Textmetadata
LicenceTDM
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.