Evidence map›Paper›PMID 26787865›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

T-cell-intrinsic Tif1α/Trim24 regulates IL-1R expression on TH2 cells and TH2 cell-mediated airway allergy.

Jimena Perez-Lloret, Isobel S Okoye, Riccardo Guidi, Yashaswini Kannan, Stephanie M Coomes, Stephanie Czieso, Gabrielle Mengus, Irwin Davidson, Mark S Wilson

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. The Immune Modulatory Role of TIF1 Proteins.Advances in experimental medicine and biology · 2024
    Review
  5. Article
  6. Article
  7. The Role of TRIM24 in Allergic Rhinitis.Allergy, asthma & immunology research · 2023
    Article
  8. Loss of TRIM24 promotes IL-10 expression via CBP/p300-dependent IFNβ1 transcription during macrophage activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. NLRP3 Ubiquitination-A New Approach to Target NLRP3 Inflammasome Activation.International journal of molecular sciences · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

9 authors at 2 institutions in 2 countries.

Jimena Perez-LloretAllergy and Anti-Helminth Immunity Laboratory, The Francis Crick Institute, Mill Hill Laboratories, London NW7 1AA, United Kingdom;
Isobel S OkoyeAllergy and Anti-Helminth Immunity Laboratory, The Francis Crick Institute, Mill Hill Laboratories, London NW7 1AA, United Kingdom;
Riccardo GuidiAllergy and Anti-Helminth Immunity Laboratory, The Francis Crick Institute, Mill Hill Laboratories, London NW7 1AA, United Kingdom;
Yashaswini KannanAllergy and Anti-Helminth Immunity Laboratory, The Francis Crick Institute, Mill Hill Laboratories, London NW7 1AA, United Kingdom;
Stephanie M CoomesAllergy and Anti-Helminth Immunity Laboratory, The Francis Crick Institute, Mill Hill Laboratories, London NW7 1AA, United Kingdom;
Stephanie CziesoAllergy and Anti-Helminth Immunity Laboratory, The Francis Crick Institute, Mill Hill Laboratories, London NW7 1AA, United Kingdom;
Gabrielle MengusDepartment of Functional Genomics and Cancer, Institut de Génétique et de Biologie Moléculaire et Cellulaire, 67400 Illkirch, France.
Irwin DavidsonDepartment of Functional Genomics and Cancer, Institut de Génétique et de Biologie Moléculaire et Cellulaire, 67400 Illkirch, France.
Mark S WilsonAllergy and Anti-Helminth Immunity Laboratory, The Francis Crick Institute, Mill Hill Laboratories, London NW7 1AA, United Kingdom; mark.wilson@crick.ac.uk.
The Francis Crick Institute · GBInstitut de génétique et de biologie moléculaire et cellulaire · FR

Funding

Cancer Research UKMedical Research Council MC_UP_A253_1028Wellcome Trust
6 · The paper itself

Abstract

There is a paucity of new therapeutic targets to control allergic reactions and forestall the rising trend of allergic diseases. Although a variety of immune cells contribute to allergy, cytokine-secreting αβ(+)CD4(+) T-helper 2 (TH2) cells orchestrate the type-2-driven immune response in a large proportion of atopic asthmatics. To identify previously unidentified putative targets in pathogenic TH2 cells, we performed in silico analyses of recently published transcriptional data from a wide variety of pathogenic TH cells [Okoye IS, et al. (2014) Proc Natl Acad Sci USA 111(30):E3081-E3090] and identified that transcription intermediary factor 1 regulator-alpha (Tif1α)/tripartite motif-containing 24 (Trim24) was predicted to be active in house dust mite (HDM)- and helminth-elicited Il4(gfp+)αβ(+)CD4(+) TH2 cells but not in TH1, TH17, or Treg cells. Testing this prediction, we restricted Trim24 deficiency to T cells by using a mixed bone marrow chimera system and found that T-cell-intrinsic Trim24 is essential for HDM-mediated airway allergy and antihelminth immunity. Mechanistically, HDM-elicited Trim24(-/-) T cells have reduced expression of many TH2 cytokines and chemokines and were predicted to have compromised IL-1-regulated signaling. Following this prediction, we found that Trim24(-/-) T cells have reduced IL-1 receptor (IL-1R) expression, are refractory to IL-1β-mediated activation in vitro and in vivo, and fail to respond to IL-1β-exacerbated airway allergy. Collectively, these data identify a previously unappreciated Trim24-dependent requirement for IL-1R expression on TH2 cells and an important nonredundant role for T-cell-intrinsic Trim24 in TH2-mediated allergy and antihelminth immunity.

Indexed as

AnimalsHelminthsHypersensitivityMiceMice, Inbred C57BLMice, TransgenicNuclear ProteinsReceptors, Interleukin-1Th2 CellsTranscription FactorsNuclear ProteinsReceptors, Interleukin-1transcriptional intermediary factor 1Transcription FactorsallergyasthmainflammationTh2Trim24

Identifiers

PMID26787865
PMCPMC4747735
OpenAlexW2262963223

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.