Evidence map›Paper›PMID 18802058›Full record

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

Activation of nonclassical CD1d-restricted NK T cells induces airway hyperreactivity in beta 2-microglobulin-deficient mice.

Youngil I Koh, Hye Young Kim, Everett H Meyer, Muriel Pichavant, Omid Akbari, Takahiro Yasumi, Paul B Savage, Rosemarie H DeKruyff, Dale T Umetsu

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

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  9. Lipid antigens in immunity.Biological chemistry · 2014
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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

9 authors at 3 institutions in 2 countries.

Youngil I Koh *Division of Immunology and Allergy, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115.
Hye Young Kim *Division of Immunology and Allergy, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115.
Everett H MeyerDivision of Immunology and Allergy, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115.
Muriel PichavantDivision of Immunology and Allergy, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115.
Omid AkbariDivision of Immunology and Allergy, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115.
Takahiro YasumiDivision of Immunology and Allergy, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115.
Paul B SavageDepartment of Chemistry and Biochemistry, Brigham Young University, Provo, UT 84602.
Rosemarie H DeKruyffDivision of Immunology and Allergy, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115.
Dale T UmetsuDivision of Immunology and Allergy, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115.
Boston Children's Hospital · USBrigham Young University · USChonnam National University · KR

Funding

MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
HETEROGENEITY AMONG HUMAN CD4+ T LYMPHOCYTESR01AI026322 · NIAID · STANFORD UNIVERSITY · PI UMETSU, DALE T · 1989 to 2010
$2.7M
THE ROLE OF TH CELL SUBSETS AND ALLERGIC LUNG INFLAMMATIR01HL062348 · NHLBI · STANFORD UNIVERSITY · PI UMETSU, DALE T · 1999 to 2007
$2.6M
NHLBI NIH HHS HL062348NHLBI NIH HHS R01 HL062348NIAID NIH HHS AI26322NIAID NIH HHS R01 AI026322NIAID NIH HHS T32 AI007290
6 · The paper itself

Abstract

Allergic asthma is characterized by Th2-driven eosinophilic airway inflammation and by a central feature called airway hyperreactivity (AHR), development of which requires the presence of classical type I invariant NK T (iNKT) cells. Allergen-induced AHR, however, develops in beta(2)-microglobulin (beta(2)m)(-/-) mice, which lack classical iNKT cells, suggesting that in some situations iNKT cells may be dispensable for the development of AHR. In contrast, our studies now suggest that a CD1d-restricted, NK1.1(+) noninvariant TCR NKT cell population is present in beta(2)m(-/-) mice and is responsible for the development of AHR but not for Th2 responses. Furthermore, treatment of beta(2)m(-/-) mice with anti-CD1d mAb or anti-NK1.1 mAb unexpectedly abolished allergen-induced AHR. The CD1-restricted NKT cells in these mice, which failed to respond to alpha-galactosylceramide and which therefore were not classical type I iNKT cells, appear to represent an NKT cell subset restricted by a beta(2)m-independent form of CD1d. These results indicate that, although classical type I iNKT cells are normally required for the development of AHR, under different circumstances other NKT cell subsets, including nonclassical NKT cells, may substitute for classical iNKT cells and induce AHR.

Indexed as

AnimalsAntigens, CD1dbeta 2-MicroglobulinBronchial HyperreactivityCells, CulturedLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNatural Killer T-CellsTh2 CellsAntigens, CD1dbeta 2-Microglobulin

Identifiers

PMID18802058
PMCPMC4884641
OpenAlexW2102675922

What OpenQuestion holds

Textmetadata
LicenceTDM
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.