The expression of IL-6, IL-6R, collagen I, collagen III, fibronectin, α-smooth muscle actin (α-SMA), and transforming growth factor (TGF-β) in TAK arteries was significantly higher than that in the normal arteries.
At baseline, median MRP8/14 levels were higher in patients with TA than healthy controls [7353 (4524 to11283) vs 4896 (3194 to 8474.5) ng/ml, p = 0.011].
In our previous study, NMR based serum metabolomics had revealed distinctive metabolic signatures in TA patients compared with age/sex matched healthy controls and systemic lupus erythematosus (SLE).
Hence, we sought evidence of B cell involvement in a large cohort of TaK by measuring serum levels of B cell survival factors activation factor (BAFF) and A proliferation inducing ligand (APRIL).
Although no definite boundaries exist, it may be suggested that the IL-6/Th17/IL-17 pathway primarily drives systemic inflammation while the IL-12/Th1/IFN-γ pathway dominates in vascular wall inflammation both in TAK and giant cell arteritis.
In CD8+ cells, two transcripts remained differentially expressed after 12 months; SGTB, associated with neuronal apoptosis, and FCGR3A, associatied with Takayasu arteritis.
At baseline, median MRP8/14 levels were higher in patients with TA than healthy controls [7353 (4524 to11283) vs 4896 (3194 to 8474.5) ng/ml, p = 0.011].
We investigated the linkage between presumptive TA-related genes (FCGR2A/FCGR3A, EEFSEC, RPS9/LILRB3, RIPPLY2 and MLX) and TA in the Han Chinese population.We performed a large case-control multi-center study of 412 Han Chinese TA patients and 597 ethnically matched healthy controls.
Regarding circulating chemokines in TA, serum/plasma levels of IL-8 (CXCL8), CCL2 and CCL5 were shown to be elevated in TA patients compared with healthy controls as well as in TA patients with active disease compared with those in remission.
Regarding circulating chemokines in TA, serum/plasma levels of IL-8 (CXCL8), CCL2 and CCL5 were shown to be elevated in TA patients compared with healthy controls as well as in TA patients with active disease compared with those in remission.
Spearman's correlation showed that ESR was correlated with PLT (r = 0.206, P = 0.020), K (r = -0.353, P < 0.001), alpha angle (r = 0.328, P < 0.001), MA (r = 0.474, P < 0.001), MA (A) (r = 0.623, P < 0.001), G (r = 0.475, P < 0.001), and TPI (r = 0.458, P < 0.001).In conclusion, inflammation was associated with platelet coagulation function rather than enzymatic coagulation function in patients with TA.
Associations between TA and serum/plasma levels of other cytokines are less clear. mRNA expression of IL-4 and tumor necrosis factor α (TNFα) are constitutively increased in peripheral blood mononuclear cells (PBMC) from TA patients and the expression of both cytokines increases even more after PBMC stimulation in vitro, while the expression of IL-10 mRNA decreases.
Regarding circulating chemokines in TA, serum/plasma levels of IL-8 (CXCL8), CCL2 and CCL5 were shown to be elevated in TA patients compared with healthy controls as well as in TA patients with active disease compared with those in remission.
A recent genome-wide association study (GWAS) has revealed that the FCGR2A/FCGR3A, EEFSEC, RPS9/LILRB3, RIPPLY2 and MLX genes confer susceptibility to TA.
Spearman's correlation showed that ESR was correlated with PLT (r = 0.206, P = 0.020), K (r = -0.353, P < 0.001), alpha angle (r = 0.328, P < 0.001), MA (r = 0.474, P < 0.001), MA (A) (r = 0.623, P < 0.001), G (r = 0.475, P < 0.001), and TPI (r = 0.458, P < 0.001).In conclusion, inflammation was associated with platelet coagulation function rather than enzymatic coagulation function in patients with TA.
Spearman's correlation showed that ESR was correlated with PLT (r = 0.206, P = 0.020), K (r = -0.353, P < 0.001), alpha angle (r = 0.328, P < 0.001), MA (r = 0.474, P < 0.001), MA (A) (r = 0.623, P < 0.001), G (r = 0.475, P < 0.001), and TPI (r = 0.458, P < 0.001).In conclusion, inflammation was associated with platelet coagulation function rather than enzymatic coagulation function in patients with TA.
These findings suggest that the polymorphisms of IL12A, IL12B, IL12RB1, IL12RB2 and IL23R might make no contribution to the susceptibility of TA in the Chinese population.
These findings suggest that the polymorphisms of IL12A, IL12B, IL12RB1, IL12RB2 and IL23R might make no contribution to the susceptibility of TA in the Chinese population.
These findings suggest that the polymorphisms of IL12A, IL12B, IL12RB1, IL12RB2 and IL23R might make no contribution to the susceptibility of TA in the Chinese population.
These findings suggest that the polymorphisms of IL12A, IL12B, IL12RB1, IL12RB2 and IL23R might make no contribution to the susceptibility of TA in the Chinese population.
These associations include ERAP1, CCR1-CCR3, STAT4, KLRC4, GIMAP4, and TNFAIP3 in Behçet's disease; BLK and CD40 in Kawasaki disease; SERPINA1 and SEMA6A in antineutrophil cytoplasmic antibody associated vasculitides; IL12B and FCGR2A/ FCGR2A in Takayasu arteritis; and CECR1 in a newly defined vascular inflammatory syndrome associated with adenosine deaminase (ADA2) deficiency.