Evidence map›Paper›PMID 21896776›Full record

ArticleInfection and immunity2011

Role of interleukin-23 (IL-23) receptor signaling for IL-17 responses in human Lyme disease.

Marije Oosting, Hadewych ter Hofstede, Frank L van de Veerdonk, Patrick Sturm, Bart-Jan Kullberg, Jos W M van der Meer, Mihai G Netea, Leo A B Joosten

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Lyme borreliosis.Nature reviews. Disease primers · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. IL-12, IL-23 and IL-17 in IBD: immunobiology and therapeutic targeting.Nature reviews. Gastroenterology & hepatology · 2019
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Interleukin 23 in Crohn's disease.Inflammatory bowel diseases · 2014
    Review
  15. Elevated levels of IL-23 in a subset of patients with post-lyme disease symptoms following erythema migrans.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2014
    Article
  16. Article
  17. Review
  18. Article
  19. Article
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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

8 authors at 2 institutions in 1 country.

Marije OostingDepartment of Medicine (463), Radboud University Nijmegen Medical Centre, Geert Grooteplein Zuid 8, 6525GA Nijmegen, The Netherlands.
Hadewych ter Hofstede
Frank L van de Veerdonk
Patrick Sturm
Bart-Jan Kullberg
Jos W M van der Meer
Mihai G Netea
Leo A B Joosten
Radboud University Nijmegen · NLRadboud University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin-23 (IL-23) is known to play a crucial role in the development and maintenance of T helper 17 cells. It has been previously demonstrated that IL-17 is involved in experimental Lyme arthritis, caused by Borrelia burgdorferi bacteria. However, the precise role of the IL-23 receptor (IL-23R) for the B. burgdorferi-induced IL-17 responses or human Lyme disease has not yet been elucidated. IL-23R single nucleotide polymorphism (SNP) rs11209026 was genotyped using the TaqMan assay. Functional studies were performed using peripheral blood mononuclear cells, and cytokines were measured using enzyme-linked immunosorbent assay (ELISA). Dose-dependent production of IL-23 and IL-17 by B. burgdorferi could be observed. Interestingly, when IL-23 bioactivity was inhibited by a specific antibody against IL-23p19, IL-17 production was significantly downregulated. In contrast, production of gamma interferon (IFN-γ) was not affected after the blockade of IL-23 activity. Moreover, individuals bearing a single nucleotide polymorphism in the IL-23R gene (Arg381Gln) produced significantly less IL-17 after B. burgdorferi stimulation compared with that of the individuals bearing the wild type. Despite lower IL-17 production, the IL-23R gene polymorphism did not influence the development of chronic Lyme disease in a cohort of patients with Lyme disease. This study demonstrates that IL-23R signaling is needed for B. burgdorferi-induced IL-17 production in vitro and that an IL-23R gene SNP leads to impaired IL-17 production. However, the IL-23R gene polymorphism is not crucial for the pathogenesis of chronic Lyme.

Indexed as

Borrelia burgdorferiChronic DiseaseGene Expression RegulationHumansInterleukin-17Leukocytes, MononuclearLyme DiseasePolymorphism, GeneticReceptors, InterleukinSignal TransductionIL23R protein, humanInterleukin-17Receptors, Interleukin

Identifiers

PMID21896776
PMCPMC3257938
OpenAlexW2110800457

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.