Association of ficolin-2 gene polymorphisms and susceptibility to systemic lupus erythematosus in Egyptian children and adolescents: a multicenter study

Abstract

Background Pediatric-onset SLE (pSLE) is a multisystem autoimmune disease. Recently, the ficolin-2 (FCN2) gene has emerged as a potential candidate gene for susceptibility to SLE. Objectives The objective of this study was to evaluate the association of the FCN2 gene polymorphisms at positions −986 (G/A), −602 (G/A), −4 (A/G) and SNP C/T (rs3124954) located in intron 1, with susceptibility to pSLE in Egyptian children and adolescents. Methods This was a multicenter study of 280 patients diagnosed with pSLE, and 280 well-matched healthy controls. The FCN2 promoter polymorphisms at –986 G/A (rs3124952), −602 G/A (rs3124953), −4 A/G (rs17514136) and SNP C/T (rs3124954) located in intron 1 were genotyped by polymerase chain reaction, while serum ficolin-2 levels were assessed using enzyme-linked immunosorbent assay. Results The frequencies of the FCN2 GG genotype and G allele at −986 and −602 positions were significantly more represented in patients with pSLE than in controls ( p < 0.001). Conversely, the FCN2 AA genotype and A allele at position −4 were more common in patients than in controls ( p < 0.001). Moreover, patients carrying the FCN2 GG genotype in −986 position were more likely to develop lupus nephritis (odds ratio: 2.6 (95% confidence interval: 1.4–4.78); p = 0.006). The FCN2 AA genotype at position −4 was also identified as a possible risk factor for lupus nephritis (odds ratio: 3.12 (95% confidence interval: 1.25–7.84); p = 0.024). Conclusion The FCN2 promoter polymorphisms may contribute to susceptibility to pSLE in Egyptian children and adolescents. Moreover, the FCN2 GG genotype at position −986 and AA genotype at position −4 were associated with low serum ficolin-2 levels and may constitute risk factors for lupus nephritis in pSLE.

Association of ficolin‐1 and ficolin‐3 gene variation and pulmonary tuberculosis susceptibility in a Chinese population

“…Ficolin‐3 is encoded by FCN3 gene on chromosome 1p36 and is secreted in plasma 14 . In recent years, many scholars had analyzed the correlation between FCN gene polymorphism and multiply autoimmune, inflammatory, and infectious diseases 14‐17 …”

“…14 In recent years, many scholars had analyzed the correlation between FCN gene polymorphism and multiply autoimmune, inflammatory, and infectious diseases. [14][15][16][17] A previous study examined the role of FCN2 gene variant in PTB 18 ; however, the FCN1 and FCN3 gene SNPs associated with PTB susceptibility had not yet been reported in Chinese population.…”