Abstract
BackgroundA previous study revealed the association between susceptibility to Takayasu arteritis (TAK) and a single nucleotide polymorphism (SNP) rs6871626 located in IL12B, which encodes interleukin (IL)-12p40, a common component of IL-12p70 and IL-23. We investigated the expression of these cytokines in patients with TAK, stratifying them into those with or without the risk allele at the rs6871626 SNP.MethodsPlasma levels of IL-12p40, IL-12p70, and IL-23 were quantified in 44 patients with TAK and 19 healthy controls (HCs) by enzyme-linked immunosorbent assays. Monocytes were obtained from 20 patients with TAK and 14 HCs, treated with interferon-γ (IFN-γ) and lipopolysaccharide, and then supernatant cytokines were quantified. In addition, the ratio of IFN-γ+ or IL-17A+ cells to CD4+ T cells was measured by flow cytometric analysis of peripheral blood mononuclear cells.ResultsThe levels of plasma IL-12p40, plasma IL-12p70, and supernatant IL-12p70 were significantly higher in patients with TAK than in HCs, whereas there were no significant differences in the levels of plasma IL-23, supernatant IL-23, or supernatant IL-12p40. The levels of plasma IL-12p70, supernatant IL-12p40, and supernatant IL-12p70 were significantly higher in patients with the risk allele than in those without. The ratio of CD4+IFN-γ+ cells was significantly higher in patients with the risk allele, whereas CD4+IL-17A+ cells showed no differences.ConclusionsThe rs6871626 SNP in IL12B may influence the increased expression of IL-12p40 and IL-12p70. These enhanced cytokines might play roles in the pathophysiology of TAK.
Highlights
A previous study revealed the association between susceptibility to Takayasu arteritis (TAK) and a single nucleotide polymorphism (SNP) rs6871626 located in IL12B, which encodes interleukin (IL)-12p40, a common component of IL-12p70 and IL-23
We previously reported that a single nucleotide polymorphism (SNP), rs6871626, in the IL12B region is associated with TAK, and that the risk allele at this SNP is correlated with clinical symptoms such as aortic regurgitation (AR) [11]
Because IL-12p70 is essential for differentiation of T helper (Th)1 cells, and IL-23 is needed for maintenance of the proportion of IL-17A+ cells (Th17) cells, we examined the proportion of Th1 and Th17 cells in the peripheral blood of patients with TAK and Healthy control (HC)
Summary
A previous study revealed the association between susceptibility to Takayasu arteritis (TAK) and a single nucleotide polymorphism (SNP) rs6871626 located in IL12B, which encodes interleukin (IL)-12p40, a common component of IL-12p70 and IL-23. Some studies have reported that innate immunity, cytokines, and genomic factors are involved in the pathophysiology of TAK. Innate immunity plays a role in tissue damage in patients with TAK. IL-6, IL-12, IL-17, and interferon-γ (IFN-γ) are highly expressed in the aortic tissues in patients with TAK [9]. These reports indicate that these cytokines play roles in the pathophysiology of TAK. Human leukocyte antigen (HLA)B*52 is associated with the onset of TAK [10]
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