Evidence map›Paper›PMID 33859636›Full record

ReviewFrontiers in immunology2021

Role of the IL23/IL17 Pathway in Crohn's Disease.

Heike Schmitt, Markus F Neurath, Raja Atreya

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed, 3 pooled it
23.0field-weighted citation impact, top 1% 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

137 citing papers in PubMed, 3 syntheses or guidelines pooled it, 186 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. Recent advances in the management of small bowel Crohn's disease.The Korean journal of internal medicine · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Type 1 and CD103European journal of immunology · 2026
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

77 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Heike SchmittFirst Department of Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Markus F NeurathFirst Department of Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Raja AtreyaFirst Department of Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Crohn's disease (CD) is a chronic relapsing disorder of the gastrointestinal tract and represents one of the main entities of inflammatory bowel disease (IBD). CD affects genetically susceptible patients that are influenced by environmental factors and the intestinal microbiome, which results in excessive activation of the mucosal immune system and aberrant cytokine responses. Various studies have implicated the pro-inflammatory cytokines IL17 and IL23 in the pathogenesis of CD. IL23 is a member of the IL12 family of cytokines and is able to enhance and affect the expansion of pathogenic T helper type 17 (Th17) cells through various mechanisms, including maintenance of Th17 signature genes, upregulation of effector genes or suppression of repressive factors. Moreover, IL17 and IL23 signaling is able to induce a cascade of pro-inflammatory molecules like TNF, IFNγ, IL22, lymphotoxin, IL1β and lipopolysaccharide (LPS). Here, IL17A and TNF are known to mediate signaling synergistically to drive expression of inflammatory genes. Recent advances in understanding the immunopathogenetic mechanisms underlying CD have led to the development of new biological therapies that selectively intervene and inhibit inflammatory processes caused by pro-inflammatory mediators like IL17 and IL23. Recently published data demonstrate that treatment with selective IL23 inhibitors lead to markedly high response rates in the cohort of CD patients that failed previous anti-TNF therapy. Macrophages are considered as a main source of IL23 in the intestine and are supposed to play a key role in the molecular crosstalk with T cell subsets and innate lymphoid cells in the gut. The following review focuses on mechanisms, pathways and specific therapies in Crohn's disease underlying the IL23/IL17 pathway.

Indexed as

AnimalsAnti-Inflammatory AgentsCell CommunicationCrohn DiseaseGastrointestinal AgentsHumansInterleukin-17Interleukin-23Intestinal MucosaMacrophagesSignal TransductionT-Lymphocyte SubsetsTumor Necrosis Factor InhibitorsAnti-Inflammatory AgentsGastrointestinal AgentsInterleukin-17Interleukin-23Tumor Necrosis Factor Inhibitorsanti-TNF therapyCrohn’s diseaseIL17/IL23 axisinflammationintestinal immunitynon-responderresistance to apoptosis

Identifiers

PMID33859636
PMCPMC8042267
OpenAlexW3143657138

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.