Role of the IL33 and IL1RL1 pathway in the pathogenesis of Immunoglobulin A vasculitis
Metadatos
Afficher la notice complèteAuteur
Prieto Peña, Diana; Sevilla Pérez, Belén; Ortego Centeno, Norberto; Márquez Ortiz, Ana; Martín, JavierEditorial
Nature
Date
2021-08-09Referencia bibliográfica
Prieto-Peña, D... [et al.]. Role of the IL33 and IL1RL1 pathway in the pathogenesis of Immunoglobulin A vasculitis. Sci Rep 11, 16163 (2021). [https://doi.org/10.1038/s41598-021-95762-5]
Patrocinador
European Commission; 'Instituto de Salud Carlos III' (ISCIII, Health Ministry, Spain) PI18/00042 Instituto de Salud Carlos III; European Social Fund (ESF) CM20/00006; RETICS Program (ISCIII) RD16/0012/0009; European Commission IDIVAL 18/01 INNVAL20/06; Servicio Cantabro de Salud; European Union FEDER fund RD16/0012/0014 PI17/00409; European Commission 734899 CP16/00033Résumé
Cytokines signalling pathway genes are crucial factors of the genetic network underlying the
pathogenesis of Immunoglobulin-A vasculitis (IgAV), an inflammatory vascular condition. An
influence of the interleukin (IL)33- IL1 receptor like (IL1RL)1 signalling pathway on the increased risk
of several immune-mediated diseases has been described. Accordingly, we assessed whether the
IL33-IL1RL1 pathway represents a novel genetic risk factor for IgAV. Three tag polymorphisms within
IL33 (rs3939286, rs7025417 and rs7044343) and three within IL1RL1 (rs2310173, rs13015714 and
rs2058660), that also were previously associated with several inflammatory diseases, were genotyped
in 380 Caucasian IgAV patients and 845 matched healthy controls. No genotypes or alleles differences
were observed between IgAV patients and controls when IL33 and IL1RL1 variants were analysed
independently. Likewise, no statistically significant differences were found in IL33 or IL1RL1 genotype
and allele frequencies when IgAV patients were stratified according to the age at disease onset or to
the presence/absence of gastrointestinal (GI) or renal manifestations. Similar results were disclosed
when IL33 and IL1RL1 haplotypes were compared between IgAV patients and controls and between