Evidence map›Paper›PMID 39139562›Full record

ArticleFrontiers in immunology2024

Inhibition of B cell receptor signaling induced by the human adenovirus species D E3/49K protein.

Andreas Hildenbrand, Precious Cramer, Milena Bertolotti, Nathalie Sophia Kaiser, Kathrin Kläsener, Clara Muriel Nickel, Michael Reth, Albert Heim, Hartmut Hengel, Hans-Gerhard Burgert and 1 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Adenoviral E3/49K: CD45-targeted immune evasion and therapeutic potential.Frontiers in cellular and infection microbiology · 2026
    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.

Andreas HildenbrandInstitute of Virology, Medical Center and Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Precious CramerInstitute of Virology, Medical Center and Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Milena BertolottiSignaling Research Centers CIBSS and BIOSS, University of Freiburg, Freiburg, Germany.
Nathalie Sophia KaiserInstitute of Virology, Medical Center and Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Kathrin KläsenerDepartment of Rheumatology and Clinical Immunology, Medical Center University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Clara Muriel NickelInstitute of Virology, Medical Center and Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Michael RethSignaling Research Centers CIBSS and BIOSS, University of Freiburg, Freiburg, Germany.
Albert HeimInstitute of Virology, Hannover Medical School, Hannover, Germany.
Hartmut HengelInstitute of Virology, Medical Center and Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Hans-Gerhard BurgertInstitute of Virology, Medical Center and Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Zsolt RuzsicsInstitute of Virology, Medical Center and Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The early transcription unit 3 (E3) of human adenoviruses (HAdVs) encodes several immunoevasins, including the E3/49K protein, which is unique for species D of HAdVs. It is expressed as surface transmembrane protein and shed. E3/49K of HAdV-D64 binds to the protein tyrosine phosphatase surface receptor CD45, thereby modulating activation of T and NK cells. Methods: Considering that E3/49K represents the most polymorphic viral protein among species D HAdVs, we demonstrate here that all tested E3/49K orthologs bind to the immunologically important regulator CD45. Thus, this feature is conserved regardless of the pathological associations of the respective HAdV types. Results: It appeared that modulation of CD45 is a unique property restricted to HAdVs of species D. Moreover, E3/49K treatment inhibited B cell receptor (BCR) signaling and impaired BCR signal phenotypes. The latter were highly comparable to B cells having defects in the expression of CD45, suggesting E3/49K as a potential tool to investigate CD45 specific functions. Conclusion: We identified B cells as new direct target of E3/49K-mediated immune modulation, representing a novel viral immunosubversive mechanism.

Indexed as

Adenovirus E3 ProteinsAdenoviruses, HumanB-LymphocytesLeukocyte Common AntigensReceptors, Antigen, B-CellSignal TransductionAdenovirus Infections, HumanHEK293 CellsHumansAdenovirus E3 ProteinsLeukocyte Common AntigensPTPRC protein, humanReceptors, Antigen, B-CelladenovirusBCR signalingCD45E3/49Kimmunoevasion

Identifiers

PMID39139562
PMCPMC11321000

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Registered trials

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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.