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AB0011 INFLUENCE OF IL17A GENE ON THE PATHOGENESIS OF IMMUNOGLOBULIN-A VASCULITIS

2020; BMJ; Volume: 79; Issue: Suppl 1 Linguagem: Inglês

10.1136/annrheumdis-2020-eular.641

1468-2060

Fernanda Genre, S. Remuzgo Martinez, Verónica Pulito‐Cueto, D. Prieto-Peña, Belén Atienza‐Mateo, B. Sevilla, Javier Llorca, N. Ortego, Leticia Lera‐Gómez, María Teresa Leonardo, Ana Peñalba, María Jesús Cabero, Luis Martín‐Penagos, José A. Miranda‐Filloy, Antonio Navas Parejo, D. de Argila, Maximiliano Aragüés, Esteban Rubio‐Romero, Manuel León Luque, J. M. Blanco-Madrigal, E. Galíndez, J. Martin Ibanez, Santos Castañeda, Ricardo Blanco, Miguel Á. González‐Gay, Raquel López‐Mejías,

IL-33, ST2, and ILC Pathways

Background: Cytokines signaling pathway genes represent a key component of the genetic network implicated in the pathogenesis of Immunoglobulin-A vasculitis (IgAV) [1], an inflammatory vascular pathology. Interleukin (IL)17A is a genetic risk locus for autoimmune diseases, such as giant cell arteritis [2] and spondyloarthritis [3]. Objectives: To determine the potential influence of IL17A on IgAV. Methods: Five IL17A tag polymorphisms (rs4711998, rs8193036, rs3819024, rs2275913 and rs7747909) were genotyped in 360 Caucasian patients with IgAV and 1,003 sex and ethnically matched healthy controls. Results: No statistically significant differences between patients with IgAV and healthy controls were observed when each IL17A genetic variant was analyzed 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. Conclusion: Our results do not support an influence of IL17A on the pathogenesis of IgAV. References: [1]Autoimmun Rev 2018; 17: 301-15 [2]Ann Rheum Dis 2014; 73: 1742-5 [3]Mediators Inflamm 2018; 2018: 1395823. Acknowledgments: This study was supported by European Union FEDER funds and “Fondo de Investigaciones Sanitarias” (grant PI18/00042) from ‘Instituto de Salud Carlos III’ (ISCIII, Health Ministry, Spain). RL-M is a recipient of a Miguel Servet type I programme fellowship from the ISCIII, co-funded by the European Social Fund (ESF, `Investing in your future´) (grant CP16/00033). SR-M is supported by funds of the RETICS Program (RD16/0012/0009) (ISCIII, co-funded by the European Regional Development Fund (ERDF)). VP-C is supported by a pre-doctoral grant from IDIVAL (PREVAL 18/01). LL-G is supported by funds of PI18/00042 (ISCIII, co-funded by ERDF). Disclosure of Interests: Fernanda Genre: None declared, Sara Remuzgo Martinez: None declared, Verónica Pulito-Cueto: None declared, D. Prieto-Peña: None declared, Belén Atienza-Mateo: None declared, Belén Sevilla: None declared, Javier Llorca: None declared, Norberto Ortego: None declared, Leticia Lera-Gómez: None declared, Maite Leonardo: None declared, Ana Peñalba: None declared, María Jesús Cabero: None declared, Luis Martín-Penagos: None declared, Jose Alberto Miranda-Filloy: None declared, Antonio Navas Parejo: None declared, Diego de Argila: None declared, Maximiliano Aragües: None declared, Esteban Rubio-Romero: None declared, MANUEL LEON LUQUE: None declared, Juan María Blanco-Madrigal: None declared, E. Galindez: None declared, Javier Martin Ibanez: None declared, Santos Castañeda: None declared, Ricardo Blanco Grant/research support from: Abbvie, MSD and Roche, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen, Lilly and MSD, Miguel A González-Gay Grant/research support from: Pfizer, Abbvie, MSD, Speakers bureau: Pfizer, Abbvie, MSD, Raquel López-Mejías: None declared