Evidence map›Paper›PMID 26694902›Full record

ArticleImmunology2016

Small molecule mediated inhibition of RORγ-dependent gene expression and autoimmune disease pathology in vivo.

Daliya Banerjee, Linlin Zhao, Lan Wu, Arumugam Palanichamy, Ayla Ergun, Liaomin Peng, Catherine Quigley, Stefan Hamann, Robert Dunstan, Patrick Cullen and 6 more

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Different Fumaric Acid Esters Elicit Distinct Pharmacologic Responses.Neurology(R) neuroimmunology & neuroinflammation · 2021
    Observational
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. RORγ regulates the NLRP3 inflammasome.The Journal of biological chemistry · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

16 authors at 1 institution in 1 country.

Daliya BanerjeeImmunology Research, Biogen, Cambridge, MA, USA.
Linlin ZhaoImmunology Research, Biogen, Cambridge, MA, USA.
Lan WuImmunology Research, Biogen, Cambridge, MA, USA.
Arumugam PalanichamyImmunology Research, Biogen, Cambridge, MA, USA.
Ayla ErgunTranslational Sciences - Genetics & Genomics, Biogen, Cambridge, MA, USA.
Liaomin PengImmunology Research, Biogen, Cambridge, MA, USA.
Catherine QuigleyTranslational Sciences - Pathology, Biogen, Cambridge, MA, USA.
Stefan HamannTranslational Sciences - Pathology, Biogen, Cambridge, MA, USA.
Robert DunstanTranslational Sciences - Pathology, Biogen, Cambridge, MA, USA.
Patrick CullenTranslational Sciences - Genetics & Genomics, Biogen, Cambridge, MA, USA.
Norm AllaireTranslational Sciences - Genetics & Genomics, Biogen, Cambridge, MA, USA.
Kevin GuertinMedicinal Chemistry, Biogen, Cambridge, MA, USA.
Tao WangMedicinal Chemistry, Biogen, Cambridge, MA, USA.
Jianhua ChaoMedicinal Chemistry, Biogen, Cambridge, MA, USA.
Christine LohImmunology Research, Biogen, Cambridge, MA, USA.
Jason D FontenotImmunology Research, Biogen, Cambridge, MA, USA.
Biogen (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoic acid receptor-related orphan nuclear receptor γ (RORγ) orchestrates a pro-inflammatory gene expression programme in multiple lymphocyte lineages including T helper type 17 (Th17) cells, γδ T cells, innate lymphoid cells and lymphoid tissue inducer cells. There is compelling evidence that RORγ-expressing cells are relevant targets for therapeutic intervention in the treatment of autoimmune and inflammatory diseases. Unlike Th17 cells, where RORγ expression is induced under specific pro-inflammatory conditions, γδ T cells and other innate-like immune cells express RORγ in the steady state. Small molecule mediated disruption of RORγ function in cells with pre-existing RORγ transcriptional complexes represents a significant and challenging pharmacological hurdle. We present data demonstrating that a novel, selective and potent small molecule RORγ inhibitor can block the RORγ-dependent gene expression programme in both Th17 cells and RORγ-expressing γδ T cells as well as a disease-relevant subset of human RORγ-expressing memory T cells. Importantly, systemic administration of this inhibitor in vivo limits pathology in an innate lymphocyte-driven mouse model of psoriasis.

Indexed as

AnimalsAutoimmune DiseasesBenzamidesCell DifferentiationDermatitisDisease Models, AnimalDose-Response Relationship, DrugGene Expression RegulationHumansImmunologic MemoryInterleukin-17MiceNuclear Receptor Subfamily 1, Group F, Member 3PyridinesReceptors, Antigen, T-Cell, gamma-deltaTh17 CellsBenzamidesBIO-0554019Interleukin-17Nuclear Receptor Subfamily 1, Group F, Member 3PyridinesReceptors, Antigen, T-Cell, gamma-deltaimiquimodROR γT helper type 17γδ T cells and autoimmunity

Identifiers

PMID26694902
PMCPMC4799885
OpenAlexW2201210340

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.