Evidence map›Paper›PMID 18941230›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Ly49h-deficient C57BL/6 mice: a new mouse cytomegalovirus-susceptible model remains resistant to unrelated pathogens controlled by the NK gene complex.

Nassima Fodil-Cornu, Seung-Hwan Lee, Simon Belanger, Andrew P Makrigiannis, Christine A Biron, R Mark Buller, Silvia M Vidal

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

74 citing papers in PubMed, 109 citations in OpenAlex.

  1. Clonal selection of somatic mutations shapes NK cell memory.bioRxiv : the preprint server for biology · 2026
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  5. Fatty acid oxidation fuels natural killer cell responses against infection and cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024
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14 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 2 countries.

Nassima Fodil-CornuDepartment of Human Genetics, McGill University, Montreal, Quebec, Canada.
Seung-Hwan Lee
Simon Belanger
Andrew P Makrigiannis
Christine A Biron
R Mark Buller
Silvia M Vidal
Brown University · USMcGill University Health Centre · CAMontreal Clinical Research Institute · CASaint Louis University · US

Funding

NATURAL KILLER CELL GROWTH AND DEVELOPMENTR01CA041268 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI BIRON, CHRISTINE A. · 1986 to 2008
$3.1M
NCI NIH HHS CA41268NCI NIH HHS R01 CA041268
6 · The paper itself

Abstract

Cmv1 was the first mouse cytomegalovirus (MCMV) resistance locus identified in C57BL/6 mice. It encodes Ly49H, a NK cell-activating receptor that specifically recognizes the m157 viral protein at the surface of MCMV-infected cells. To dissect the effect of the Ly49h gene in host-pathogen interactions, we generated C57BL/6 mice lacking the Ly49h region. We found that 36 h after MCMV infection, the lack of Ly49h resulted in high viral replication in the spleen and dramatically enhanced proinflammatory cytokine production in the serum and spleen. At later points in time, we observed that MCMV induced a drastic loss in CD8(+) T cells in B6.Ly49h(-/-) mice, probably reflecting severe histological changes in the spleen. Overall, our results indicate that Ly49H(+) NK cells contain a systemic production of cytokines that may contribute to the MCMV-induced pathology and play a central role in maintaining normal spleen cell microarchitecture. Finally, we tested the ability of B6.Ly49h(-/-) mice to control replication of Leishmania major and ectromelia virus. Resistance to these pathogens has been previously mapped within the NK gene complex. We found that the lack of Ly49H(+) NK cells is not associated with an altered resistance to L. major. In contrast, absence of Ly49H(+) NK cells seems to afford additional protection against ectromelia infection in C57BL/6 mice, suggesting that Ly49H may recognize ectromelia-infected cells with detrimental effects. Taken together, these results confirm the pivotal role of the Ly49H receptor during MCMV infection and open the way for further investigations in host-pathogen interactions.

Indexed as

AnimalsBase SequenceCHO CellsCricetinaeCricetulusCytokinesDisease Models, AnimalEctromelia virusGenetic Predisposition to DiseaseHerpesviridae InfectionsImmunity, InnateLeishmania majorMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred StrainsCytokinesKlra8 protein, mouseNK Cell Lectin-Like Receptor Subfamily AReceptors, Natural Killer Cell

Identifiers

PMID18941230
PMCPMC4485379
OpenAlexW1520347430

What OpenQuestion holds

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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.