Evidence map›Paper›PMID 17565608›Full record

ArticleClinical and experimental immunology2007

Linkage between Toll-like receptor (TLR) 2 promotor and intron polymorphisms: functional effects and relevance to sarcoidosis.

M Veltkamp, P A H M Wijnen, C H M van Moorsel, G T Rijkers, H J T Ruven, M Heron, O Bekers, A M E Claessen, M Drent, J M M van den Bosch and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
  2. Review
  3. Immune mechanisms in fibrotic pulmonary sarcoidosis.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  4. Innate and Adaptive Immunity in Noninfectious Granulomatous Lung Disease.Journal of immunology (Baltimore, Md. : 1950) · 2022
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Etiologies of Sarcoidosis.Clinical reviews in allergy & immunology · 2015
    Review
  11. Article
  12. Sarcoidosis vs. Sarcoid-like reactions: The Two Sides of the same Coin?Wiener medizinische Wochenschrift (1946) · 2014
    Review
  13. Immune dysfunction in cirrhosis.World journal of gastroenterology · 2014
    Review
  14. Interleukin-12 family cytokines and sarcoidosis.Frontiers in pharmacology · 2014
    Review
  15. Granuloma formation in pulmonary sarcoidosis.Frontiers in immunology · 2013
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

11 authors at 2 institutions in 1 country.

M VeltkampHeart Lung Center Utrecht, Department of Pulmonology, St. Antonius Hospital, Nieuwegein, The Netherlands. veltkamp76@hotmail.com
P A H M Wijnen
C H M van Moorsel
G T Rijkers
H J T Ruven
M Heron
O Bekers
A M E Claessen
M Drent
J M M van den Bosch
J C Grutters
St. Antonius Ziekenhuis · NLMaastricht University Medical Centre · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intracellular pathogens Propionibacterium acnes and Mycobacterium tuberculosis have been leading suspects as the cause of sarcoidosis, a systemic disorder characterized by the formation of non-caseating granulomas. Toll-like receptor (TLR) 2 is important in the innate immune response against both pathogens, and is therefore of interest in sarcoidosis research. In the present study, three single nucleotide polymorphisms and one dinucleotide repeat polymorphism in the TLR-2 gene were genotyped in 419 sarcoidosis patients, divided into a study cohort and a validation cohort, and 196 healthy controls. In the study cohort we found a significant increase in prevalence of the AA-genotype at promotor location -16934 in patients with chronic disease compared to patients with acute/self-remitting sarcoidosis (34.5% versus 15.9%, respectively, P = 0.006, P(c) = 0.019). These results could not be confirmed in our validation cohort, implicating a possible role for TLR-2 genetics in only a small percentage of sarcoidosis patients. Furthermore, linkage was found between the promotor polymorphism -16934 A/T and the number of GT repeats in intron 1 (P < 0.0001). After in vitro stimulation of peripheral blood mononuclear cells (PMBCs) with different TLR-2 agonists, a correlation between induction of TNF-alpha (P = 0.008), interleukin (IL)-12 (P = 0.008) as well as IL-6 (P = 0.02), and the number of GT repeats was observed. In conclusion, the data show that polymorphisms in TLR-2 might be important in a small group of sarcoidosis patients and that their functional consequences explain partly some of the variance in cytokine pattern observed in different clinical phenotypes of this disease.

Indexed as

Polymorphism, GeneticAcute DiseaseChronic DiseaseCytokinesFemaleGenetic LinkageHumansIntronsMalePolymorphism, Single NucleotidePromoter Regions, GeneticSarcoidosisSeverity of Illness IndexToll-Like Receptor 2CytokinesTLR2 protein, humanToll-Like Receptor 2

Identifiers

PMID17565608
PMCPMC2219322
OpenAlexW1585126227

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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.