Evidence map›Paper›PMID 12871214›Full record

ArticleImmunology2003

Hepatitis B virus-induced defect of monocyte-derived dendritic cells leads to impaired T helper type 1 response in vitro: mechanisms for viral immune escape.

Susanne Beckebaum, Vito R Cicinnati, Xia Zhang, Stanislav Ferencik, Andrea Frilling, Hans Grosse-Wilde, Christoph Erich Broelsch, Guido Gerken

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 138 citations in OpenAlex.

  1. Review
  2. Article
  3. Unveiling low level viremia in chronic hepatitis B: challenges and new horizons.Frontiers in cellular and infection microbiology · 2025
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Reactivation rates in patients using biological agents, with resolved HBV infection or isolated anti-HBc IgG positivity.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2018
    Article
  16. Article
  17. Article
  18. Immune Response in Hepatitis B Virus Infection.Cold Spring Harbor perspectives in medicine · 2015
    Review
  19. Review
  20. 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

8 authors at 1 institution in 1 country.

Susanne BeckebaumDepartment of Gastroenterology and Hepatology, Department of General Surgery and Transplantation, and Institute of Immunology, University of Essen, Germany.
Vito R Cicinnati
Xia Zhang
Stanislav Ferencik
Andrea Frilling
Hans Grosse-Wilde
Christoph Erich Broelsch
Guido Gerken
Essen University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendritic cells (DC) are the most potent antigen-presenting cells and play a central role in the induction of antiviral immune responses. Recently, we have shown that monocyte-derived DC (MoDC) from patients with chronic hepatitis B virus (HBV) infection are functionally impaired. In our present study MoDC from healthy subjects were propagated in vitro and inoculated with HBV particles to investigate the precise mechanisms that underly MoDC dysfunction. T-cell proliferation assays revealed an impaired allostimulatory capacity of HBV-inoculated MoDC (HBV-MoDC) as well as a lower potential of stimulating autologous T cells against a recall antigen in comparison to control-MoDC. Interleukin-2, tumour necrosis factor-alpha and interferon-gamma production by T cells in proliferation assays with HBV-MoDC was significantly lower than with control-MoDC and correlated with lower IL-12 production in HBV-MoDC cultures. The presence of the nucleoside analogue lamivudine (3TC), an inhibitor of HBV replication, restored impaired allostimulatory function of HBV-MoDC and up-regulated major histocompatibility complex class II expression. These results show that HBV infection compromises the antigen-presenting function of MoDC with concomitant impairment of T helper cell type 1 responses. This may play an important role for viral immune escape leading to chronic HBV infection. However, 3TC treatment can overcome HBV-MoDC-related T-cell hyporeactivity and this underscores its important role in enhanced immune responses to HBV.

Indexed as

AdultApoptosisCells, CulturedDendritic CellsEndocytosisFemaleHepatitis B virusHLA-DR AntigensHumansInterferon-gammaInterleukin-12Interleukin-2LamivudineLymphocyte Culture Test, MixedMaleMonocytesHLA-DR AntigensInterferon-gammaInterleukin-12Interleukin-2LamivudineTetanus ToxoidTumor Necrosis Factor-alpha

Identifiers

PMID12871214
PMCPMC1783010
OpenAlexW1998597340

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.