Evidence map›Paper›PMID 31386594›Full record

ReviewAnnual review of pharmacology and toxicology2020

(Inverse) Agonists of Retinoic Acid-Related Orphan Receptor γ: Regulation of Immune Responses, Inflammation, and Autoimmune Disease.

Anton M Jetten, Donald N Cook

Open access · bronzeAbstract readReview
In one paragraph

Review in Annual review of pharmacology and toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 77 citations in OpenAlex.

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  18. The effect ofMolecular biology research communications · 2023
    Article
  19. Review
  20. The application of machine learning methods to the prediction of novel ligands for RORComputational and structural biotechnology journal · 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

2 authors at 2 institutions in 1 country.

Anton M JettenCell Biology Section, Immunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA; email: jetten@niehs.nih.gov.
Donald N CookImmunogenetics Section, Immunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA.
National Institute of Environmental Health Sciences · USNational Institutes of Health · US

Funding

Allergic sensitization through the airwayZIAES102025 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI COOK, DONALD N · 2009 to 2025
$32.6M
Nuclear receptors: action, functions, and roles in diseaseZIAES101586 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI JETTEN, ANTON M · 2009 to 2025
$13.5M
Mechanism Of Action And Functions Of The Gli-related Proteins Glis 1-3Z01ES100485 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI JETTEN, ANTON M · 2002 to 2008
$2.3M
Intramural NIH HHS Z01 ES100485Intramural NIH HHS ZIA ES102025NIEHS NIH HHS ZIA ES102025
6 · The paper itself

Abstract

Retinoic acid-related orphan receptor γt (RORγt) functions as a ligand-dependent transcription factor that regulates multiple proinflammatory genes and plays a critical role in several inflammatory and autoimmune diseases. Various endogenous and synthetic RORγ (inverse) agonists have been identified that regulate RORγ transcriptional activity, including many cholesterol intermediates and oxysterols. Changes in cholesterol biosynthesis and metabolism can therefore have a significant impact on the generation of oxysterol RORγ ligands and, consequently, can control RORγt activity and inflammation. These observations contribute to a growing literature that connects cholesterol metabolism to the regulation of immune responses and autoimmune disease. Loss of RORγ function in knockout mice and in mice treated with RORγ inverse agonists results in reduced production of proinflammatory cytokines, such as IL-17A/F, and increased resistance to autoimmune disease in several experimental rodent models. Thus, RORγt inverse agonists might provide an attractive therapeutic approach to treat a variety of autoimmune diseases.

Indexed as

AnimalsAutoimmune DiseasesCytokinesDisease Models, AnimalDrug Inverse AgonismHumansInflammationLigandsMiceMice, KnockoutNuclear Receptor Subfamily 1, Group F, Member 3CytokinesLigandsNuclear Receptor Subfamily 1, Group F, Member 3autoimmune diseasecholesterol biosynthesisinflammation(inverse) agonistsretinoic acid–related orphan receptorRORγTh17 cells

Identifiers

PMID31386594
PMCPMC6952538
OpenAlexW2964526505

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.