Evidence map›Paper›PMID 31000797›Full record

ReviewGenes and immunity2019

The IL-23/IL-17 pathway in human chronic inflammatory diseases-new insight from genetics and targeted therapies.

Elisabetta Bianchi, Lars Rogge

Abstract readReview
PubMed Publisher
In one paragraph

Review in Genes and immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Dissecting PGENature communications · 2026
    Article
  4. Article
  5. Article
  6. Interpreting the Function of the IL-23/IL-17 Axis through Bioinformatics.Endocrine, metabolic & immune disorders drug targets · 2025
    Review
  7. Review
  8. Guselkumab binding to CD64Frontiers in immunology · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. A machine-learning based bio-psycho-social model for the prediction of non-obstructive and obstructive coronary artery disease.Clinical research in cardiology : official journal of the German Cardiac Society · 2023
    Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Molecular Targets and Mechanisms ofEvidence-based complementary and alternative medicine : eCAM · 2021
    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 1 institution in 1 country.

Elisabetta BianchiImmunoregulation Unit, Department of Immunology, Institut Pasteur, Paris, France.
Lars RoggeImmunoregulation Unit, Department of Immunology, Institut Pasteur, Paris, France. lars.rogge@pasteur.fr.ORCID http://orcid.org/0000-0003-1262-9204
Institut Pasteur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, spondyloarthritis, and psoriasis cause significant morbidity and are a considerable burden for the patients in terms of pain, impaired function, and diminished quality of life, as well as for society, because of the associated high health-care costs and loss of productivity. Our limited understanding of the pathogenic mechanisms involved in these diseases currently hinders early diagnosis and the development of more specific and effective therapies. The past years have been marked by considerable progress in our insight of the genetic basis of many diseases. In particular, genome-wide association studies (GWAS) performed with thousands of patients have provided detailed information about the genetic variants associated with a large number of chronic inflammatory diseases. These studies have brought to the forefront many genes linked to signaling pathways that were not previously known to be involved in pathogenesis, pointing to new directions in the study of disease mechanisms. GWAS also provided fundamental evidence for a key role of the immune system in the pathogenesis of these diseases, because many of the identified loci map to genes involved in different immune processes. However, the mechanisms by which disease-associated genetic variants act on disease development and the targeted cell populations remain poorly understood. The challenge of the post-GWAS era is to understand how these variants affect pathogenesis, to allow translation of genetic data into better diagnostics and innovative treatment strategies. Here, we review recent results that document the importance of the IL-23/IL-17 pathway for the pathogenesis of several chronic inflammatory diseases and summarize data that demonstrate how therapeutic targeting of this pathway can benefit affected patients.

Indexed as

Genetic Predisposition to DiseaseAnimalsAntibodies, MonoclonalAnti-Inflammatory AgentsHumansImmune System DiseasesInterleukin-17Interleukin-23Antibodies, MonoclonalAnti-Inflammatory AgentsInterleukin-17Interleukin-23

Identifiers

PMID31000797
OpenAlexW2936175126

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.