PReS-FINAL-2113: The association of the NFKB1 gene polymorphism with systemic onset juvenile idiopathic arthritis in Russia

Va Malievsky,Kv Danilko,Ls Nazarova,Tv Viktorova

doi:10.1186/1546-0096-11-s2-p125

Va Malievsky, Kv Danilko + Show 2 more

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https://doi.org/10.1186/1546-0096-11-s2-p125

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Abstract

Juvenile idiopathic arthritis (JIA) is a childhood onset autoimmune disorder characterized by inflammation of joints and other tissues. The basis for susceptibility to common autoimmune and inflammatory diseases, including JIA, is a complex interplay between multiple genetic and environmental risk factors. NF-κb appears to be a central player in several autoimmune diseases, according to recent studies of genetic defects in autoreactive lymphoid cells in both murine models of autoimmunity and humans with diverse forms of autoimmunity. Meta-analysis suggested a possible association between NFKB1 -94 ins/delattg promoter polymorphism and certain autoimmune and inflammatory diseases in the Asian population, but not in the Caucasian population.

Highlights

Juvenile idiopathic arthritis (JIA) is a childhood onset autoimmune disorder characterized by inflammation of joints and other tissues
No differences were observed in allele and genotype frequencies of the NFKB1 -94 ins/del ATTG polymorphism between total JIA patients and controls
Stratification analysis across all ILAR subgroups revealed only weak association of the ins*ins* genotype with systemic onset (SO) in comparison to all others JIA types (c2 = 4,014, p = 0,045, odds ratio (OR) = 3,063, 95% CI 1,1278,324)

Summary

Introduction

Juvenile idiopathic arthritis (JIA) is a childhood onset autoimmune disorder characterized by inflammation of joints and other tissues. The basis for susceptibility to common autoimmune and inflammatory diseases, including JIA, is a complex interplay between multiple genetic and environmental risk factors. NF-b appears to be a central player in several autoimmune diseases, according to recent studies of genetic defects in autoreactive lymphoid cells in both murine models of autoimmunity and humans with diverse forms of autoimmunity. Meta-analysis suggested a possible association between NFKB1 -94 ins/delattg promoter polymorphism and certain autoimmune and inflammatory diseases in the Asian population, but not in the Caucasian population

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