HLA-DRB1*04 was associated with increased risk for RA and ACPA positivity, while HLA-DRB1*07 was associated with reduced risk for RA and RF synthesis in Algerian patients.
Background
The B-cell lymphocyte kinase (BLK) is a src family protein tyrosine kinase expressed in B-lineage cells. BLK gene polymorphism was reported as a risk factor in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) susceptibility.
Objectives
To investigate whether the association of BLK gene polymorphism with RA is present in an Algerian population.
Methods
The BLK (rs13277113) single nucleotide polymorphism was directly genotyped in 223 RA patients and 200 healthy controls by real time -polymerase chain reaction method (TaqMan Assays). The relationships between anti-citrullinated peptide antibody (ACPA) positivity, rheumatoid factor (RF) positivity and BLK genotypes were analyzed statistically. Disease activity score (DAS28) and HAQ score were also assessed.
Results
Significant associations between RA and controls were observed for AG heterozygote genotype (21% vs 33%, P=0.004, OR=0.53) and recessive model (AA vs. AG+GG, 94% vs 99%, P=0.002, OR=0.08). Allele frequencies did not differ between patients and controls and between antibodies positive (ACPA, RF) and negative RA (P>0.05). No significant difference in genotypes distribution was found after stratification according to parameters of disease activity (DAS 28 and HAQ, P>0.05).
Conclusions
Our result indicates that polymorphism in BLK gene is associated with susceptibility to RA in Algerian population but not with the severity.
References
Génin E, Coustet B, Allanore Y, et al. Epistatic interaction between BANK1 and BLK in rheumatoid arthritis: results from a large trans-ethnic meta-analysis. PLoS One. 2013 Apr 30;8(4)
Viatte S, Plant D, Bowes J, et al. Genetic markers of rheumatoid arthritis susceptibility in anti-citrullinated peptide antibody negative patients. Ann Rheum Dis. 2012 Dec;71(12)
Zhang H, Wang L, Huang Y, et al. Influence of BLK polymorphisms on the risk of rheumatoid arthritis. Mol Biol Rep. 2012 Nov;39(11).
Disclosure of Interest
None declared
DOI
10.1136/annrheumdis-2014-eular.1943
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