Evidence map›Paper›PMID 34813654›Full record

ArticleThe Journal of experimental medicine2021

ACC1-expressing pathogenic T helper 2 cell populations facilitate lung and skin inflammation in mice.

Takahiro Nakajima, Toshio Kanno, Satoru Yokoyama, Shigemi Sasamoto, Hikari K Asou, Damon J Tumes, Osamu Ohara, Toshinori Nakayama, Yusuke Endo

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. CCR8The Journal of allergy and clinical immunology · 2026
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  12. NRF2 is a spatiotemporal metabolic hub essential for the polyfunctionality of Th2 cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. T helper 2 cells in asthma.The Journal of experimental medicine · 2023
    Review
  19. Review
  20. Characterization of proteogenomic signatures of differentiation of CD4+ T cell subsets.DNA research : an international journal for rapid publication of reports on genes and genomes · 2023
    Article
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.

Takahiro NakajimaDepartment of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, Chiba, Japan.ORCID 0000-0002-4564-469X
Toshio KannoDepartment of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, Chiba, Japan.ORCID 0000-0002-7586-8723
Satoru YokoyamaDepartment of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, Chiba, Japan.ORCID 0000-0001-6051-0043
Shigemi SasamotoDepartment of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, Chiba, Japan.ORCID 0000-0001-9358-5674
Hikari K AsouDepartment of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, Chiba, Japan.ORCID 0000-0002-2701-5953
Damon J TumesCentre for Cancer Biology, University of South Australia, North Terrace, Adelaide, Australia.ORCID 0000-0001-5709-857X
Osamu OharaDepartment of Applied Genomics Kazusa DNA Research Institute, Chiba, Japan.ORCID 0000-0002-3328-9571
Toshinori NakayamaDepartment of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-1434-2007
Yusuke EndoDepartment of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, Chiba, Japan.ORCID 0000-0002-7223-1938
Kazusa DNA Research Institute · JPChiba University · JPUniversity of South Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T cells possess distinguishing effector functions and drive inflammatory disorders. We have previously identified IL-5-producing Th2 cells as the pathogenic population predominantly involved in the pathology of allergic inflammation. However, the cell-intrinsic signaling pathways that control the pathogenic Th2 cell function are still unclear. We herein report the high expression of acetyl-CoA carboxylase 1 (ACC1) in the pathogenic CD4+ T cell population in the lung and skin. The genetic deletion of CD4+ T cell-intrinsic ACC1 dampened eosinophilic and basophilic inflammation in the lung and skin by constraining IL-5 or IL-3 production. Mechanistically, ACC1-dependent fatty acid biosynthesis induces the pathogenic cytokine production of CD4+ T cells via metabolic reprogramming and the availability of acetyl-CoA for epigenetic regulation. We thus identified a distinct phenotype of the pathogenic T cell population in the lung and skin, and ACC1 was shown to be an essential regulator controlling the pathogenic function of these populations to promote type 2 inflammation.

Indexed as

Acetyl-CoA CarboxylaseAdministration, TopicalAnimalsBasophilsCalcitriolCD4-Positive T-LymphocytesDrug EruptionsFatty AcidsGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-3Interleukin-5MiceMice, Inbred BALB CMice, Inbred C57BLMice, Mutant StrainsPneumoniaACC1 protein, mouseAcetyl-CoA CarboxylasecalcipotrieneCalcitriolFatty AcidsGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-3Interleukin-5

Identifiers

PMID34813654
PMCPMC8614157
OpenAlexW3215615684

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.