Evidence map›Paper›PMID 26680205›Full record

ArticleImmunity2015

The Inhibitory Receptor NKG2A Sustains Virus-Specific CD8⁺ T Cells in Response to a Lethal Poxvirus Infection.

Aaron S Rapaport, Jill Schriewer, Susan Gilfillan, Ed Hembrador, Ryan Crump, Beatrice F Plougastel, Yaming Wang, Gaelle Le Friec, Jian Gao, Marina Cella and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
2.1field-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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
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  18. Natural Immunomodulatory Agents as a Complementary Therapy for Poxviruses.Advances in experimental medicine and biology · 2024
    Review
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  20. Article

1 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

14 authors at 3 institutions in 2 countries.

Aaron S RapaportDepartment of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA.
Jill SchriewerDepartment of Molecular Microbiology and Immunology, Saint Louis University Health Sciences Center, 1402 South Grand Blvd, St. Louis, MO 63104, USA.
Susan GilfillanDepartment of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA.
Ed HembradorDepartment of Molecular Microbiology and Immunology, Saint Louis University Health Sciences Center, 1402 South Grand Blvd, St. Louis, MO 63104, USA.
Ryan CrumpDepartment of Molecular Microbiology and Immunology, Saint Louis University Health Sciences Center, 1402 South Grand Blvd, St. Louis, MO 63104, USA.
Beatrice F PlougastelRheumatology Division, Department of Medicine, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA.
Yaming WangDepartment of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA.
Gaelle Le FriecDepartment of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA.
Jian GaoRheumatology Division, Department of Medicine, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA.
Marina CellaDepartment of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA.
Hanspeter PircherInstitute of Immunology, Center for Microbiology and Hygiene, University Medical Center Freiburg, Hermann-Herder Strasse 11, 79104 Freiburg, Germany.
Wayne M YokoyamaRheumatology Division, Department of Medicine, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA; Howard Hughes Medical Institute, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA.
R Mark L BullerDepartment of Molecular Microbiology and Immunology, Saint Louis University Health Sciences Center, 1402 South Grand Blvd, St. Louis, MO 63104, USA.
Marco ColonnaDepartment of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA. Electronic address: mcolonna@pathology.wustl.edu.
Washington University in St. Louis · USSaint Louis University · USUniversity Medical Center Freiburg · DE

Funding

Infectious Diseases/Basic Microbial Pathogenic MechanismsT32AI007172 · NIAID · WASHINGTON UNIVERSITY · PI Daniel E. Goldberg, JENNIFER A PHILIPS · 1985 to 2026
$13.0M
Viral Discovery in Rheumatoid ArthritisP30AR048335 · NIAMS · WASHINGTON UNIVERSITY · PI YOKOYAMA, WAYNE M. · 2001 to 2015
$8.9M
INHIBITORY RECEPTORS IN IMMUNITY AGAINST LETHAL ACUTE VIRUS INFECTIONR56AI119083 · NIAID · WASHINGTON UNIVERSITY · PI COLONNA, MARCO · 2015 to 2015
$381k
Howard Hughes Medical InstituteNIAID NIH HHS 1R56AI119083-01NIAID NIH HHS HHSN272201300006CNIAID NIH HHS R56 AI119083NIAID NIH HHS T32 AI007172NIAID NIH HHS T32-AI007172NIAMS NIH HHS P30 AR048335NIAMS NIH HHS P30-AR048335PHS HHS HHSN272201300006C
6 · The paper itself

Abstract

CD8(+) T cells and NK cells protect from viral infections by killing virally infected cells and secreting interferon-γ. Several inhibitory receptors limit the magnitude and duration of these anti-viral responses. NKG2A, which is encoded by Klrc1, is a lectin-like inhibitory receptor that is expressed as a heterodimer with CD94 on NK cells and activated CD8(+) T cells. Previous studies on the impact of CD94/NKG2A heterodimers on anti-viral responses have yielded contrasting results and the in vivo function of NKG2A remains unclear. Here, we generated Klrc1(-/-) mice and found that NKG2A is selectively required for resistance to ectromelia virus (ECTV). NKG2A functions intrinsically within ECTV-specific CD8(+) T cells to limit excessive activation, prevent apoptosis, and preserve the specific CD8(+) T cell response. Thus, although inhibitory receptors often cause T cell exhaustion and viral spreading during chronic viral infections, NKG2A optimizes CD8(+) T cell responses during an acute poxvirus infection.

Indexed as

AnimalsCD8-Positive T-LymphocytesCytotoxicity, ImmunologicDisease Models, AnimalFlow CytometryKiller Cells, NaturalMiceMice, Inbred C57BLMice, KnockoutNK Cell Lectin-Like Receptor Subfamily COligonucleotide Array Sequence AnalysisPoxviridae InfectionsReal-Time Polymerase Chain ReactionNK Cell Lectin-Like Receptor Subfamily CCD8(+) T cellcytokineinhibitory receptorNK cellNKG2Avirus

Identifiers

PMID26680205
PMCPMC4745883
OpenAlexW2195237963

What OpenQuestion holds

Textmetadata
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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.