Evidence map›Paper›PMID 18367531›Full record

ArticleJournal of virology2008

Subdominant CD8 T-cell epitopes account for protection against cytomegalovirus independent of immunodomination.

Rafaela Holtappels, Christian O Simon, Michael W Munks, Doris Thomas, Petra Deegen, Birgit Kühnapfel, Torsten Däubner, Simone F Emde, Jürgen Podlech, Natascha K A Grzimek and 3 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
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  5. Article
  6. Human rhinovirus-specific CD8 T cell responses target conserved and unusual epitopes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
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  10. Review
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  17. Review
  18. Article
  19. T cell responses to cytomegalovirus.Nature reviews. Immunology · 2016
    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

13 authors at 2 institutions in 2 countries.

Rafaela HoltappelsInstitute for Virology, Johannes Gutenberg University, Hochhaus am Augustusplatz, 55131 Mainz, Germany. R.Holtappels-Geginat@uni-mainz.de
Christian O Simon
Michael W Munks
Doris Thomas
Petra Deegen
Birgit Kühnapfel
Torsten Däubner
Simone F Emde
Jürgen Podlech
Natascha K A Grzimek
Silke A Oehrlein-Karpi
Ann B Hill
Matthias J Reddehase
Johannes Gutenberg University Mainz · DEOregon Health & Science University · US

Funding

INTERACTIONS AT THE MICROBE/HOST INTERFACET32AI007472 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI LANDFEAR, SCOTT M · 1995 to 2019
$6.7M
The CD8 T cell response to murine cytomegalovirusR01AI047206 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI HILL, ANN B · 2002 to 2015
$4.6M
MECHANISM OF MCMV's INHIBITION OF ANTIGEN PRESENTATIONR01AI050099 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI HILL, ANN B · 2002 to 2006
$1.2M
NIAID NIH HHS 5T32 AI007472NIAID NIH HHS R01 AI047206NIAID NIH HHS R01 AI050099NIAID NIH HHS R01 AI47206NIAID NIH HHS R01 AI50099NIAID NIH HHS T32 AI007472
6 · The paper itself

Abstract

Cytomegalovirus (CMV) infection continues to be a complication in recipients of hematopoietic stem cell transplantation (HSCT). Preexisting donor immunity is recognized as a favorable prognostic factor for the reconstitution of protective antiviral immunity mediated primarily by CD8 T cells. Furthermore, adoptive transfer of CMV-specific memory CD8 T (CD8-T(M)) cells is a therapeutic option for preventing CMV disease in HSCT recipients. Given the different CMV infection histories of donor and recipient, a problem may arise from an antigenic mismatch between the CMV variant that has primed donor immunity and the CMV variant acquired by the recipient. Here, we have used the BALB/c mouse model of CMV infection in the immunocompromised host to evaluate the importance of donor-recipient CMV matching in immundominant epitopes (IDEs). For this, we generated the murine CMV (mCMV) recombinant virus mCMV-DeltaIDE, in which the two memory repertoire IDEs, the IE1-derived peptide 168-YPHFMPTNL-176 presented by the major histocompatibility complex class I (MHC-I) molecule L(d) and the m164-derived peptide 257-AGPPRYSRI-265 presented by the MHC-I molecule D(d), are both functionally deleted. Upon adoptive transfer, polyclonal donor CD8-T(M) cells primed by mCMV-DeltaIDE and the corresponding revertant virus mCMV-revDeltaIDE controlled infection of immunocompromised recipients with comparable efficacy and regardless of whether or not IDEs were presented in the recipients. Importantly, CD8-T(M) cells primed under conditions of immunodomination by IDEs protected recipients in which IDEs were absent. This shows that protection does not depend on compensatory expansion of non-IDE-specific CD8-T(M) cells liberated from immunodomination by the deletion of IDEs. We conclude that protection is, rather, based on the collective antiviral potential of non-IDEs independent of the presence or absence of IDE-mediated immunodomination.

Indexed as

Adoptive TransferAnimalsCD8-Positive T-LymphocytesCells, CulturedDisease Models, AnimalEpitopes, T-LymphocyteFemaleFibroblastsHerpesviridae InfectionsImmunodominant EpitopesKineticsMiceMice, Inbred BALB CMuromegalovirusViral ProteinsEpitopes, T-LymphocyteImmunodominant EpitopesViral Proteins

Identifiers

PMID18367531
PMCPMC2395166
OpenAlexW2163855681

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.