Evidence map›Paper›PMID 24023637›Full record

ArticlePloS one2013

Gender-specific effects of genetic variants within Th1 and Th17 cell-mediated immune response genes on the risk of developing rheumatoid arthritis.

Rafael Cáliz, Luz María Canet, Carmen Belén Lupiañez, Helena Canhão, Alejandro Escudero, Ileana Filipescu, Juana Segura-Catena, María José Soto-Pino, Manuela Expósito-Ruiz, Miguel Ángel Ferrer and 10 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Differences in IDO1Frontiers in immunology · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. C-type lectins in immunity and homeostasis.Nature reviews. Immunology · 2018
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. 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

20 authors at 8 institutions in 3 countries.

Rafael CálizRheumatology Department, Virgen de las Nieves University Hospital, Granada, Spain.
Luz María Canet
Carmen Belén Lupiañez
Helena Canhão
Alejandro Escudero
Ileana Filipescu
Juana Segura-Catena
María José Soto-Pino
Manuela Expósito-Ruiz
Miguel Ángel Ferrer
Antonio García
Lurdes Romani
Alfonso González-Utrilla
Teresa Vallejo
Eva Pérez-Pampin
Kari Hemminki
Asta Försti
Eduardo Collantes
João Eurico Fonseca
Juan Sainz
Hospital Universitario Virgen de las Nieves · ESHospital Universitario Reina Sofía · ESPfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research · ESHeidelberg University · DEGerman Cancer Research Center · DEHospital de Santa Maria · PTInstituto de Investigación Sanitaria de Santiago · ESUniversity of Lisbon · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study was conducted to explore whether single nucleotide polymorphisms (SNPs) in Th1 and Th17 cell-mediated immune response genes differentially influence the risk of rheumatoid arthritis (RA) in women and men. In phase one, 27 functional/tagging polymorphisms in C-type lectins and MCP-1/CCR2 axis were genotyped in 458 RA patients and 512 controls. Carriers of Dectin-2 rs4264222T allele had an increased risk of RA (OR = 1.47, 95%CI 1.10-1.96) whereas patients harboring the DC-SIGN rs4804803G, MCP-1 rs1024611G, MCP-1 rs13900T and MCP-1 rs4586C alleles had a decreased risk of developing the disease (OR = 0.66, 95%CI 0.49-0.88; OR = 0.66, 95%CI 0.50-0.89; OR = 0.73, 95%CI 0.55-0.97 and OR = 0.68, 95%CI 0.51-0.91). Interestingly, significant gender-specific differences were observed for Dectin-2 rs4264222 and Dectin-2 rs7134303: women carrying the Dectin-2 rs4264222T and Dectin-2 rs7134303G alleles had an increased risk of RA (OR = 1.93, 95%CI 1.34-2.79 and OR = 1.90, 95%CI 1.29-2.80). Also five other SNPs showed significant associations only with one gender: women carrying the MCP-1 rs1024611G, MCP-1 rs13900T and MCP-1 rs4586C alleles had a decreased risk of RA (OR = 0.61, 95%CI 0.43-0.87; OR = 0.67, 95%CI 0.47-0.95 and OR = 0.60, 95%CI 0.42-0.86). In men, carriers of the DC-SIGN rs2287886A allele had an increased risk of RA (OR = 1.70, 95%CI 1.03-2.78), whereas carriers of the DC-SIGN rs4804803G had a decreased risk of developing the disease (OR = 0.53, 95%CI 0.32-0.89). In phase 2, we genotyped these SNPs in 754 RA patients and 519 controls, leading to consistent gender-specific associations for Dectin-2 rs4264222, MCP-1 rs1024611, MCP-1 rs13900 and DC-SIGN rs4804803 polymorphisms in the pooled sample (OR = 1.38, 95%CI 1.08-1.77; OR = 0.74, 95%CI 0.58-0.94; OR = 0.76, 95%CI 0.59-0.97 and OR = 0.56, 95%CI 0.34-0.93). SNP-SNP interaction analysis of significant SNPs also showed a significant two-locus interaction model in women that was not seen in men. This model consisted of Dectin-2 rs4264222 and Dectin-2 rs7134303 SNPs and suggested a synergistic effect between the variants. These findings suggest that Dectin-2, MCP-1 and DC-SIGN polymorphisms may, at least in part, account for gender-associated differences in susceptibility to RA.

Indexed as

Genetic Predisposition to DiseaseSex CharacteristicsArthritis, RheumatoidCell Adhesion MoleculesChemokine CCL2DC-Specific ICAM-3 Grabbing NonintegrinDectin-1DemographyFemaleHumansImmunity, CellularLectins, C-TypeMaleMiddle AgedMultifactor Dimensionality ReductionPolymorphism, Single NucleotideCCL2 protein, humanCCR2 protein, humanCell Adhesion MoleculesChemokine CCL2CLEC7A protein, humanDC-Specific ICAM-3 Grabbing NonintegrinDectin-1dectin-2, mouseLectins, C-TypeReceptors, CCR2Receptors, Cell Surface

Identifiers

PMID24023637
PMCPMC3758336
OpenAlexW2167641406

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.