Evidence map›Paper›PMID 10432280›Full record

ArticleThe Journal of experimental medicine1999

Molecular mimicry of human cytochrome P450 by hepatitis C virus at the level of cytotoxic T cell recognition.

A R Kammer, S H van der Burg, B Grabscheid, I P Hunziker, K M Kwappenberg, J Reichen, C J Melief, A Cerny

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 152 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. [Advances in clinical diagnosis and treatment of autoimmune liver diseases combined with viral hepatitis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Review
  7. Hepatitis C Virus and Molecular Mimicry.Pathogens (Basel, Switzerland) · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. Autoimmune hepatitis: current challenges and future prospects.Clinical and experimental gastroenterology · 2017
    Review
  12. Article
  13. Article
  14. Causation by HEV of extrahepatic manifestations remains unproven.Liver international : official journal of the International Association for the Study of the Liver · 2016
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

8 authors at 2 institutions in 2 countries.

A R KammerDepartment of Internal Medicine, University Hospital, Inselspital, 3010 Bern, Switzerland.
S H van der Burg
B Grabscheid
I P Hunziker
K M Kwappenberg
J Reichen
C J Melief
A Cerny
University Hospital of Bern · CHLeiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) is thought to be involved in the pathogenesis of autoimmune hepatitis (AIH) type 2, which is defined by the presence of type I antiliver kidney microsome autoantibodies directed mainly against cytochrome P450 (CYP)2D6 and by autoreactive liver infiltrating T cells. Virus-specific CD8(+) cytotoxic T lymphocytes (CTLs) that recognize infected cells and contribute to viral clearance and tissue injury during HCV infection could be involved in the induction of AIH. To explore whether the antiviral cellular immunity may turn against self-antigens, we characterized the primary CTL response against an HLA-A*0201-restricted HCV-derived epitope, i.e., HCV core 178-187, which shows sequence homology with human CYP2A6 and CYP2A7 8-17. To determine the relevance of these homologies for the pathogenesis of HCV-associated AIH, we used synthetic peptides to induce primary CTL responses in peripheral blood mononuclear cells of healthy blood donors and patients with chronic HCV infection. We found that the naive CTL repertoire of both groups contains cross-reactive CTLs inducible by the HCV peptide recognizing both CYP2A6 and CYP2A7 peptides as well as endogenously processed CYP2A6 protein. Importantly, we failed to induce CTLs with the CYP-derived peptides that showed a lower capacity to form stable complexes with the HLA-A2 molecule. These findings demonstrate the potential of HCV to induce autoreactive CD8(+) CTLs by molecular mimicry, possibly contributing to virus-associated autoimmunity.

Indexed as

Aryl Hydrocarbon HydroxylasesMolecular MimicryAmino Acid SequenceAutoimmunityCD8-Positive T-LymphocytesCross ReactionsCytochrome P-450 CYP2A6Cytochrome P-450 Enzyme SystemEpitopesHepacivirusHepatitis CHepatitis C AntigensHLA-A2 AntigenHumansLiverMixed Function OxygenasesAryl Hydrocarbon HydroxylasesCYP2A6 protein, humanCytochrome P-450 CYP2A6Cytochrome P-450 Enzyme SystemEpitopesHepatitis C AntigensHLA-A2 AntigenMixed Function Oxygenases

Identifiers

PMID10432280
PMCPMC2195568
OpenAlexW2078231720

What OpenQuestion holds

Textmetadata
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.