Evidence map›Paper›PMID 30104382›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

Interleukin 4 is inactivated via selective disulfide-bond reduction by extracellular thioredoxin.

Nicholas M Plugis, Nielson Weng, Qinglan Zhao, Brad A Palanski, Holden T Maecker, Aida Habtezion, Chaitan Khosla

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Classification of Protein Disulfide Bonds.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Autonomous Non Antioxidant Roles forFrontiers in cellular and infection microbiology · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  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

7 authors at 1 institution in 1 country.

Nicholas M PlugisDepartment of Chemistry, Stanford University, Stanford, CA 94305.
Nielson WengDepartment of Chemistry, Stanford University, Stanford, CA 94305.
Qinglan ZhaoDivision of Gastroenterology and Hepatology, Department of Medicine, School of Medicine, Stanford University, Stanford, CA 94305.
Brad A PalanskiDepartment of Chemistry, Stanford University, Stanford, CA 94305.
Holden T MaeckerInstitute for Immunity, Transplantation and Infection, Stanford University, Stanford, CA 94305.
Aida HabtezionDivision of Gastroenterology and Hepatology, Department of Medicine, School of Medicine, Stanford University, Stanford, CA 94305.
Chaitan KhoslaDepartment of Chemistry, Stanford University, Stanford, CA 94305; khosla@stanford.edu.
Stanford University · US

Funding

Role of Transglutaminase 2 in Celiac SprueR01DK063158 · NIDDK · STANFORD UNIVERSITY · PI CHAITAN KHOSLA · 2003 to 2026
$11.2M
Role of immune cells in chronic pancreatitisR01DK105263 · NIDDK · STANFORD UNIVERSITY · PI HABTEZION, AIDA · 2016 to 2020
$2.2M
NIDDK NIH HHS R01 DK063158NIDDK NIH HHS R01 DK105263
6 · The paper itself

Abstract

Thioredoxin 1 (TRX), an essential intracellular redox regulator, is also secreted by mammalian cells. Recently, we showed that TRX activates extracellular transglutaminase 2 via reduction of an allosteric disulfide bond. In an effort to identify other extracellular substrates of TRX, macrophages derived from THP-1 cells were treated with NP161, a small-molecule inhibitor of secreted TRX. NP161 enhanced cytokine outputs of alternatively activated macrophages, suggesting that extracellular TRX regulated the activity of interleukin 4 (IL-4) and/or interleukin 13 (IL-13). To test this hypothesis, the C35S mutant of human TRX was shown to form a mixed disulfide bond with recombinant IL-4 but not IL-13. Kinetic analysis revealed a

Indexed as

AnimalsDisease Models, AnimalDisulfidesHumansInterleukin-13Interleukin-4Mass SpectrometryMiceOxidation-ReductionPancreatitisThioredoxinsTHP-1 CellsDisulfidesIL4 protein, humanInterleukin-13Interleukin-4ThioredoxinsTxn1 protein, mousedisulfide bondinterleukin 4M2macrophagesthioredoxin

Identifiers

PMID30104382
PMCPMC6126747
OpenAlexW2885779585

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.