Evidence map›Paper›PMID 15746081›Full record

ArticleBlood2005

IFN-gamma-mediated negative feedback regulation of NKT-cell function by CD94/NKG2.

Tsuyoshi Ota, Kazuyoshi Takeda, Hisaya Akiba, Yoshihiro Hayakawa, Kouetsu Ogasawara, Yoshinori Ikarashi, Sachiko Miyake, Hiro Wakasugi, Takashi Yamamura, Mitchell Kronenberg and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 57 citations in OpenAlex.

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  13. β-mannosylceramide activates type I natural killer t cells to induce tumor immunity without inducing long-term functional anergy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
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  19. NKG2A inhibits invariant NKT cell activation in hepatic injury.Journal of immunology (Baltimore, Md. : 1950) · 2009
    Article
  20. 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

15 authors at 1 institution in 3 countries.

Tsuyoshi OtaDepartment of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
Kazuyoshi Takeda
Hisaya Akiba
Yoshihiro Hayakawa
Kouetsu Ogasawara
Yoshinori Ikarashi
Sachiko Miyake
Hiro Wakasugi
Takashi Yamamura
Mitchell Kronenberg
David H Raulet
Katsuyuki Kinoshita
Hideo Yagita
Mark J Smyth
Ko Okumura
La Jolla Institute for Immunology · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of invariant natural killer T (iNKT) cells with CD1d-restricted T-cell receptor (TCR) ligands is a powerful means to modulate various immune responses. However, the iNKT-cell response is of limited duration and iNKT cells appear refractory to secondary stimulation. Here we show that the CD94/NKG2A inhibitory receptor plays a critical role in down-regulating iNKT-cell responses. Both TCR and NK-cell receptors expressed by iNKT cells were rapidly down-modulated by priming with alpha-galactosylceramide (alpha-GalCer) or its analog OCH [(2S,3S,4R)-1-O-(alpha-D-galactopyranosyl)-N-tetracosanoyl-2-amino-1,3,4-nonanetriol)]. TCR and CD28 were re-expressed more rapidly than the inhibitory NK-cell receptors CD94/NKG2A and Ly49, temporally rendering the primed iNKT cells hyperreactive to ligand restimulation. Of interest, alpha-GalCer was inferior to OCH in priming iNKT cells for subsequent restimulation because alpha-GalCer-induced interferon gamma (IFN-gamma) up-regulated Qa-1b expression and Qa-1b in turn inhibited iNKT-cell activity via its interaction with the inhibitory CD94/NKG2A receptor. Blockade of the CD94/NKG2-Qa-1b interaction markedly augmented recall and primary responses of iNKT cells. This is the first report to show the critical role for NK-cell receptors in controlling iNKT-cell responses and provides a novel strategy to augment the therapeutic effect of iNKT cells by priming with OCH or blocking of the CD94/NKG2A inhibitory pathway in clinical applications.

Indexed as

AnimalsAntibodies, MonoclonalAntigens, CDFeedback, PhysiologicalGalactosylceramidesHistocompatibility Antigens Class IImmunologic MemoryInterferon-gammaKiller Cells, NaturalLectins, C-TypeLigandsLymphocyte ActivationMiceMice, Inbred C57BLMice, Mutant StrainsNK Cell Lectin-Like Receptor Subfamily Calpha-galactosylceramideAntibodies, MonoclonalAntigens, CDGalactosylceramidesHistocompatibility Antigens Class IInterferon-gammaKlrc1 protein, mouseKlrd1 protein, mouseLectins, C-TypeLigandsNK Cell Lectin-Like Receptor Subfamily CNK Cell Lectin-Like Receptor Subfamily DQ surface antigensReceptors, ImmunologicReceptors, Natural Killer Cell

Identifiers

PMID15746081
PMCPMC1895133
OpenAlexW2140179235

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.