In:
The Journal of Rheumatology, The Journal of Rheumatology, Vol. 39, No. 1 ( 2012-01), p. 135-140
Abstract:
Interleukin 23 (IL-23) stimulates the differentiation of T helper 17 (Th17) cells, which are involved in the pathogenesis of ankylosing spondylitis (AS). Binding of IL-23 to the IL-23 receptor complex activates Janus kinases 2 and tyrosine kinase 2, which phosphorylate IL-23R and subsequently promote the transcription of the IL-17 gene. IL-12B encodes a p40 subunit common to IL-12 and IL-23. We evaluated the effects of IL-12B and IL-23R genotype on the occurrence and clinical features of AS. Methods. A total of 362 patients with AS and 362 healthy controls were enrolled in the study. Genotypes of IL-12B A1188C (rs3212227) and IL-23R C2370A (rs10889677) were identified by polymerase chain reaction/restriction fragment-length polymorphism. Disease activity and functional status were assessed by Bath AS indices. Results. Subjects carrying IL-12B CC [matched relative risk (RR m ) 1.93, 95% CI 1.23–3.03] and IL-12B AC (RR m 1.73, 95% CI 1.21–2.46) genotypes had a significantly greater risk of developing AS than subjects with the IL-12B AA genotype. Subjects carrying both IL-12B CC and IL-23R AA genotypes also had a significantly higher risk (RR m 2.98, 95% CI 1.51–5.89) of developing AS compared to those with IL-12B AA and IL-23R CC/CA genotypes, and this interaction between IL-12B and IL-23R was significant. Patients with AS who had IL-12B CC and IL-12B AC genotypes had an obviously increased Bath Ankylosing Spondylitis Disease Activity Index score compared to those who carried the IL-12B AA genotype (4.3 vs 3.7). Conclusion. The IL-12B A1188C genotype was associated with the development and disease severity of AS.
Type of Medium:
Online Resource
ISSN:
0315-162X
,
1499-2752
DOI:
10.3899/jrheum.110613
Language:
English
Publisher:
The Journal of Rheumatology
Publication Date:
2012
