Evidence map›Paper›PMID 32582572›Full record

ArticleFrontiers in cellular and infection microbiology2020

Enhancement of Antigen Presentation by Deletion of Viral Immune Evasion Genes Prevents Lethal Cytomegalovirus Disease in Minor Histocompatibility Antigen-Mismatched Hematopoietic Cell Transplantation.

Emin Gezinir, Jürgen Podlech, Kerstin M Gergely, Sara Becker, Matthias J Reddehase, Niels A W Lemmermann

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Emin GezinirInstitute for Virology and Research Center for Immunotherapy (FZI) at the University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Jürgen PodlechInstitute for Virology and Research Center for Immunotherapy (FZI) at the University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Kerstin M GergelyInstitute for Virology and Research Center for Immunotherapy (FZI) at the University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Sara BeckerInstitute for Virology and Research Center for Immunotherapy (FZI) at the University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Matthias J ReddehaseInstitute for Virology and Research Center for Immunotherapy (FZI) at the University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Niels A W LemmermannInstitute for Virology and Research Center for Immunotherapy (FZI) at the University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematoablative treatment followed by hematopoietic cell transplantation (HCT) for reconstituting the co-ablated immune system is a therapeutic option to cure aggressive forms of hematopoietic malignancies. In cases of family donors or unrelated donors, immunogenetic mismatches in major histocompatibility complex (MHC) and/or minor histocompatibility (minor-H) loci are unavoidable and bear a risk of graft-vs.-host reaction and disease (GvHR/D). Transient immunodeficiency inherent to the HCT protocol favors a productive reactivation of latent cytomegalovirus (CMV) that can result in multiple-organ CMV disease. In addition, there exists evidence from a mouse model of MHC class-I-mismatched GvH-HCT to propose that mismatches interfere with an efficient reconstitution of antiviral immunity. Here we used a mouse model of MHC-matched HCT with C57BL/6 donors and MHC-congenic BALB.B recipients that only differ in polymorphic autosomal background genes, including minor-H loci coding for minor-H antigens (minor-HAg). Minor-HAg mismatch is found to promote lethal CMV disease in absence of a detectable GvH response to an immunodominant minor-HAg, the

Indexed as

Cytomegalovirus InfectionsHematopoietic Stem Cell TransplantationAnimalsAntigen PresentationCD8-Positive T-LymphocytesCytomegalovirusImmune EvasionMiceMice, Inbred C57BLMinor Histocompatibility AntigensMinor Histocompatibility Antigensbone marrow transplantationCD8 T cellsgraft-vs.-host disease (GvHD)hematopoietic reconstitutionminor histocompatibility antigensmurine cytomegalovirusnodular inflammatory focus (NIF)transplantation tolerance

Identifiers

PMID32582572
PMCPMC7296086
OpenAlexW3034848222

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.