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Small-vessel vasculitis

 

Influence of IL17A gene on the pathogenesis of immunoglobulin-A vasculitis

1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25

 

  1. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain. rlopezmejias78@gmail.com
  2. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
  3. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
  4. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
  5. Division of Paediatrics, Hospital Universitario San Cecilio, Granada, Spain.
  6. Epidemiology and Computational Biology Department, School of Medicine, Universidad de Cantabria, and CIBER Epidemiología y Salud Pública (CIBERESP), IDIVAL, Santander, Spain.
  7. Systemic Autoimmune Diseases Unit, Hospital Universitario San Cecilio, Granada, Spain.
  8. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
  9. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
  10. Division of Paediatrics, Hospital Universitario Marqués de Valdecilla, Santander, Spain.
  11. Division of Paediatrics, Hospital Universitario Marqués de Valdecilla, Santander, Spain.
  12. Division of Paediatrics, Hospital Universitario Marqués de Valdecilla, Santander, Spain.
  13. Nephrology Department, Hospital Universitario Marqués de Valdecilla, IDIVAL-REDINREN, Santander, Spain.
  14. Division of Rheumatology, Hospital Universitario Lucus Augusti, Lugo, Spain.
  15. Nephrology Department, Hospital Universitario San Cecilio, Granada, Spain.
  16. Dermatology Department, Hospital Universitario de La Princesa, IIS-Princesa, Madrid, Spain.
  17. Dermatology Department, Hospital Universitario de La Princesa, IIS-Princesa, Madrid, Spain.
  18. Rheumatology Department, Hospital Universitario Virgen del Rocío, Sevilla, Spain.
  19. Rheumatology Department, Hospital Universitario Virgen del Rocío, Sevilla, Spain.
  20. Rheumatology Department, Hospital Universitario de Basurto, Bilbao, Spain.
  21. Rheumatology Department, Hospital Universitario de Basurto, Bilbao, Spain.
  22. Instituto de Parasitología y Biomedicina ‘López-Neyra’, CSIC, PTS Granada, Granada, Spain.
  23. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
  24. Rheumatology Department, Hospital Universitario de La Princesa, IIS-Princesa, Madrid, Spain.
  25. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander; Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa; and Universidad de Cantabria, Santander, Spain. miguelaggay@hotmail.com

CER12930
2020 Vol.38, N°2 ,Suppl.124
PI 0166, PF 0170
Small-vessel vasculitis

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PMID: 32242803 [PubMed]

Received: 07/11/2019
Accepted : 03/02/2020
In Press: 25/03/2020
Published: 21/05/2020

Abstract

OBJECTIVES:
Cytokines signaling pathway genes represent a key component of the genetic network implicated in the pathogenesis of immunoglobulin-A vasculitis (IgAV), an inflammatory vascular pathology. Interleukin (IL)17A is described as a genetic risk locus for some autoimmune diseases, such as giant cell arteritis and spondyloarthritis. Accordingly, we aimed to determine the potential influence of IL17A on the pathogenesis of IgAV.
METHODS:
Five IL17A tag polymorphisms (rs4711998, rs8193036, rs3819024, rs2275913 and rs7747909), which cover the major variability of this gene, were genotyped in 360 Caucasian patients with IgAV and 1,003 sex and ethnically matched healthy controls using TaqMan probes.
RESULTS:
No statistically significant differences between patients with IgAV and healthy controls were observed when each IL17A genetic variant was analysed independently. Similarly, no statistically significant differences between patients with IgAV and healthy controls were found when the five IL17A polymorphisms were evaluated combined conforming haplotypes. In addition, there were no statistically significant differences in genotype, allele and haplotype frequencies of IL17A when patients with IgAV were stratified according to the age at disease onset or to the presence/absence of gastrointestinal or renal manifestations.
CONCLUSIONS:
Our results do not support an influence of IL17A on the pathogenesis of IgAV.

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