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

Autores de IDIVAL

• 

  Raquel López Mejías

  Autor

• 

  Fernanda Genre Romero

  Autor

• Sara Remuzgo Martínez

  Autor

• 

  Verónica Pulito Cueto

  Autor

• Javier Llorca Díaz

  Autor

• Verónica Mijares Díaz

  Autor

• Leticia Lera Gomez

  Autor

• María Teresa Leonardo Cabello

  Autor

• Ana Peñalba Citores

  Autor

• 

  María Jesús Cabero Pérez

  Autor

• 

  Luis Martín Penagos

  Autor

• Jose Alberto Miranda Filloy

  Autor

• 

  Ricardo Blanco Alonso

  Autor

• Miguel Ángel González-Gay Mantecón

  Autor

Autores ajenos al IDIVAL

• Sevilla-Perez, B
• Ortego-Centeno, N
• Parejo, AN
• Perez, JS
• de Argila, D
• Rubio, E
• Luque, ML
• Blanco-Madrigal, JM
• Galindez-Agirregoikoa, E
• Martin, J
• Castaneda, S

Unidades

• EPIDEMIOLOGÍA Y SALUD PÚBLICA

  

  Investigador Responsable

  Trinidad Dierssen Sotos

• INMUNOPATOLOGÍA

  

  Investigador Corresponsable

  Ricardo Blanco Alonso

Abstract

Objective. Cytokines signalling 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 r renal manifestations. Conclusion. Our results do not support an influence of IL17A on the pathogenesis of IgAV.

Keywords

• IgA; IL17A; vasculitis