No evidence of association between functional polymorphisms located within IL6R and IL6ST genes and Henoch–Schönlein purpura. Issue 6 (December 2013)

• Record Type: Journal Article
• Authors: López‐Mejías, R.; Sevilla Pérez, B.; Genre, F.; Castañeda, S.; Ortego‐Centeno, N.; Llorca, J.; Ubilla, B.; Ochoa, R.; Pina, T.; Marquez, A.; Sala‐Icardo, L.; Miranda‐Filloy, J. A.; Rueda‐Gotor, J.; Martín, J.; Blanco, R.; González‐Gay, M. A.
• Is Part Of: Tissue antigens. Volume 82:Issue 6(2013)
• Page Start: 416
• Page End: 419
• Publication Date: 2013-12
• Subjects: Antigens -- Periodicals; Immunological tolerance -- Periodicals; Immunogenetics -- Periodicals; 571.9645
• DOI: 10.1111/tan.12251
• Languages: English
• ISSNs: 0001-2815

Abstract

<abstract abstract-type="main" id="tan12251-abs-0001"> <title>Abstract</title> <p id="tan12251-para-0001">Henoch–Schönlein purpura (HSP) is the most common type of primary small‐sized blood vessel vasculitis in children and an uncommon condition in adults. Interleukin (IL)‐6 is a proinflammatory cytokine whose effect is controlled by the IL‐6 receptor (IL‐6R). IL‐6 transducer (IL‐6ST/gp130) is the signal‐transducing subunit of the IL‐6R. Two hundred and eighty five Spanish HSP patients and 877 sex and ethnically matched controls were genotyped for the <italic>IL6R</italic> rs2228145 and <italic>IL6ST/gp130</italic> rs2228044 functional polymorphisms. No significant differences in the genotype and allele frequencies between HSP patients and controls were observed. Moreover, there were no differences between HSP patients according to the age at disease onset, presence of nephritis or gastrointestinal manifestations. Our results do not confirm association of <italic>IL6R</italic> rs2228145 and <italic>IL6ST/gp130</italic> rs2228044 polymorphisms with HSP.</p> </abstract>