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Objectives  To determine whether the interleukin-33 (IL-33)-interleukin-1 receptor like 1 (IL-1RL1) signaling pathway is implicated in the risk of subclinical atherosclerosis in patients with rheumatoid arthritis (RA).    Methods  A total of 576 Spanish RA patients from Northern Spain were genotyped for 6 well-known  IL33-IL1RL1  polymorphisms ( IL33  rs3939286,  IL33  rs7025417,  IL33  rs7044343,  IL1RL1  rs2058660,  IL1RL1  rs2310173 and  IL1RL1  rs13015714) by TaqMan genotyping assay. The presence of subclinical atherosclerosis was determined by the assessment of carotid intima-media thickness (cIMT) by carotid ultrasound (US).    Results  RA patients carrying the TT genotype of the  IL33  rs3939286 polymorphism had lower cIMT values than those homozygous for the CC genotype (mean ± standard deviation (SD): 0.71 ± 0.14 mm  versus  0.76 ± 0.16 mm, respectively) while patients carrying the CT genotype had intermediate cIMT values (mean ± SD: 0.73 ± 0.17 mm). Moreover, RA patients carrying the mutant allele T of the  IL33  rs3939286 polymorphism exhibited significantly lower cIMT values than those carrying the wild allele C (mean ± SD: 0.72 ± 0.16 mm  versus  0.75 ± 0.18 mm respectively; p = 0.04). The association of both genotype and allele frequencies of  IL33  rs3939286 and cIMT levels remained statistically significant after adjustment for sex, age at the time of US study, follow-up and center (p = 0.006 and p = 0.0023, respectively), evidencing that the potential effect conferred by  IL33  rs3939286 may be independent of confounder factors. No association with other  IL33-IL1RL1  genetic variants was observed.    Conclusions  In conclusion, our results may suggest a potential protective effect of the  IL33  rs3939286 allele T in the risk of subclinical atherosclerosis in patients with RA.

Protective Role of the Interleukin 33 rs3939286 Gene Polymorphism in the Development of Subclinical Atherosclerosis in Rheumatoid Arthritis Patients