Evidence map›Paper›PMID 22346732›Full record

ArticlePLoS biology2012

Development and function of invariant natural killer T cells producing T(h)2- and T(h)17-cytokines.

Hiroshi Watarai, Etsuko Sekine-Kondo, Tomokuni Shigeura, Yasutaka Motomura, Takuwa Yasuda, Rumi Satoh, Hisahiro Yoshida, Masato Kubo, Hiroshi Kawamoto, Haruhiko Koseki and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed, 1 pooled it
9.3field-weighted citation impact, top 1% 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

132 citing papers in PubMed, 1 synthesis or guideline pooled it, 200 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Markers and makers of NKT17 cells.Experimental & molecular medicine · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

72 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

11 authors at 3 institutions in 2 countries.

Hiroshi WataraiLaboratory for Immune Regulation, RIKEN Research Center for Allergy and Immunology, Kanagawa, Japan. hwatarai@rcai.riken.jp
Etsuko Sekine-Kondo
Tomokuni Shigeura
Yasutaka Motomura
Takuwa Yasuda
Rumi Satoh
Hisahiro Yoshida
Masato Kubo
Hiroshi Kawamoto
Haruhiko Koseki
Masaru Taniguchi
RIKEN Center for Integrative Medical Sciences · JPImmune Regulation (United Kingdom) · GBTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is heterogeneity in invariant natural killer T (iNKT) cells based on the expression of CD4 and the IL-17 receptor B (IL-17RB), a receptor for IL-25 which is a key factor in T(H)2 immunity. However, the development pathway and precise function of these iNKT cell subtypes remain unknown. IL-17RB⁺iNKT cells are present in the thymic CD44⁺/⁻ NK1.1⁻ population and develop normally even in the absence of IL-15, which is required for maturation and homeostasis of IL-17RB⁻iNKT cells producing IFN-γ. These results suggest that iNKT cells contain at least two subtypes, IL-17RB⁺ and IL-17RB⁻ subsets. The IL-17RB⁺iNKT subtypes can be further divided into two subtypes on the basis of CD4 expression both in the thymus and in the periphery. CD4⁺ IL-17RB⁺iNKT cells produce T(H)2 (IL-13), T(H)9 (IL-9 and IL-10), and T(H)17 (IL-17A and IL-22) cytokines in response to IL-25 in an E4BP4-dependent fashion, whereas CD4⁻ IL-17RB⁺iNKT cells are a retinoic acid receptor-related orphan receptor (ROR)γt⁺ subset producing T(H)17 cytokines upon stimulation with IL-23 in an E4BP4-independent fashion. These IL-17RB⁺iNKT cell subtypes are abundantly present in the lung in the steady state and mediate the pathogenesis in virus-induced airway hyperreactivity (AHR). In this study we demonstrated that the IL-17RB⁺iNKT cell subsets develop distinct from classical iNKT cell developmental stages in the thymus and play important roles in the pathogenesis of airway diseases.

Indexed as

AnimalsBronchial HyperreactivityCells, CulturedCytokinesFlow CytometryGene Expression ProfilingImmunophenotypingLiverLungMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutNatural Killer T-CellsOrgan SpecificityReceptors, Interleukin-17CytokinesReceptors, Interleukin-17

Identifiers

PMID22346732
PMCPMC3274505
OpenAlexW1975975357

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.