Role of IRF5 in the pathogenesis of immunoglobulin-A vasculitis

Autores de IDIVAL

• 

  Fernanda Genre Romero

  Autor

• Sara Remuzgo Martínez

  Autor

• 

  Diana Prieto Peña

  Autor

• 

  Belén Atienza Mateo

  Autor

• 

  Verónica Pulito Cueto

  Autor

• Javier Llorca 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

• 

  Raquel López Mejías

  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
• Gualillo, O
• Martin, J
• Castaneda, S

Unidades

• EPIDEMIOLOGÍA Y SALUD PÚBLICA

  

  Investigador Responsable

  Trinidad Dierssen Sotos

• INMUNOPATOLOGÍA

  

  Investigador Corresponsable

  Ricardo Blanco Alonso

Abstract

Objective. Interferon regulatory factor 5 (IRF5) is a major regulator of type I interferon induction and is also critical to produce pro-inflammatory cytokines. An influence of IRF5 genetic variants on the increased risk of immune-mediated diseases has been described. Accordingly, we aimed to evaluate the implication of IRF5 in the pathogenesis of Immunoglobulin-A vasculitis (IgAV), an inflammatory vascular pathology. Methods. Three tag genetic variants (rs2004640, rs2070197 and rs10954213),representative of 3 different haplotve blocks within IRF5, were genotyped in 372 Caucasian patients with IgAV and 876 sex and ethnically matched healthy controls by TaqMan assays. Results. No significant differences in the genotype and allele,frequencies between patients with IgAV and healthy controls were observed when each IRF5 polymorphism was evaluated independently. Likewise, no significant differences between patients with IgAV and healthy controls were found when we assessed the three IRE:5 polymorphisms combined, conforming haplotypes. In addition, there were no significant differences in genotype, allele and haplotype frequencies of IRE:5 when patients with IgAV were stratified according to the age at disease onset or to the presence/absence of gastrointestinal or renal manifestations. Conclusion. Our results do not support an influence of IRF5 on the pathogenesis of IgAV.

Keywords

• IgA; vasculitis; IRF5