Takayasu arteritis risk locus in <i>IL6</i> might increase disease susceptibility by suppression of the anti-inflammatory gene <i>GPNMB</i> through chromatin looping and recruitment of MEF2-HDAC epigenetic repressive complex.
Both serum PTX-3 and LAMP-2 levels were elevated in TAK patients compared with those in healthy controls (PTX- 3: 0.32±0.03 ng/ml vs. 0.18±0.02 ng/ ml, p=0.001; LAMP-2: 4.40±0.14 ng/ ml vs. 3.30±0.20 ng/ml, p<0.001).
We revealed preferential recruitment of myocyte enhancer factor 2-histone deacetylase (MEF2-HDAC) repressive complex to the Takayasu arteritis risk allele.
Considering this, we further built a logistic regression model based on multiple cytokines, including CA (cancer antigen) 125, FLRG (follistatin-related protein), IGFBP (insulin-like growth factor-binding protein)-2, CA15-3, GROa (growth-regulated alpha protein), LYVE (lymphatic vessel endothelial hyaluronic acid receptor)-1, ULBP (UL16-binding protein)-2, and CD (cluster of differentiation) 99, with an area under the curve reaching 0.909 for discriminating TA activity status.
Among the subsets of VAs, serum HMGB1 levels were significantly higher in AAV, polyarteritis nodosa (PAN) and takayasu arteritis (TA) than in HC (all P < .05).
To investigate serum levels of a panel of angiogenic inducers (VEGF, FGF-2, Angiopoietin 1, -2, soluble VCAM-1) and inhibitors (angiostatin, endostatin, pentraxin-3) in patients with giant cell arteritis (GCA) and Takayasu's arteritis (TAK), in order to gain further insights into the molecular mechanisms driving angiogenesis dysregulation in large-vessel vasculitis (LVV).
<i>Aim</i>: To investigate the relation between polymorphisms in the interleukin 10 (<i>IL</i>)-<i>10</i>, tumor necrosis factor (<i>TNF)</i>-α, transforming growth factor (<i>TGF)-</i>β and interferon (<i>IFN)-γ</i> genes and Takayasu's arteritis in the Mexican population.
To investigate serum levels of a panel of angiogenic inducers (VEGF, FGF-2, Angiopoietin 1, -2, soluble VCAM-1) and inhibitors (angiostatin, endostatin, pentraxin-3) in patients with giant cell arteritis (GCA) and Takayasu's arteritis (TAK), in order to gain further insights into the molecular mechanisms driving angiogenesis dysregulation in large-vessel vasculitis (LVV).
<i>Aim</i>: To investigate the relation between polymorphisms in the interleukin 10 (<i>IL</i>)-<i>10</i>, tumor necrosis factor (<i>TNF)</i>-α, transforming growth factor (<i>TGF)-</i>β and interferon (<i>IFN)-γ</i> genes and Takayasu's arteritis in the Mexican population.
The mRNA expression of S100A8, S100A9, S100A12 and TLR4 were higher, while expression of RAGE and HSP70 were lower in TA as compared to healthy controls.
The mRNA expression of S100A8, S100A9, S100A12 and TLR4 were higher, while expression of RAGE and HSP70 were lower in TA as compared to healthy controls.
Aim of this study was to examine the expression of TLR4 and its endogenous ligands in peripheral blood mononuclear cells (PBMCs) of patients with Takayasu arteritis (TA).
The mRNA expression of S100A8, S100A9, S100A12 and TLR4 were higher, while expression of RAGE and HSP70 were lower in TA as compared to healthy controls.
Considering this, we further built a logistic regression model based on multiple cytokines, including CA (cancer antigen) 125, FLRG (follistatin-related protein), IGFBP (insulin-like growth factor-binding protein)-2, CA15-3, GROa (growth-regulated alpha protein), LYVE (lymphatic vessel endothelial hyaluronic acid receptor)-1, ULBP (UL16-binding protein)-2, and CD (cluster of differentiation) 99, with an area under the curve reaching 0.909 for discriminating TA activity status.
RESULTS In patients with Takayasu arteritis, the erythrocyte sedimentation rate (ESR), CRP, CRP/albumin ratio, red cell distribution width (RDW), neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), and monocyte-lymphocyte ratio (MLR) were significantly higher, and albumin and MPV were significantly lower compared with controls.
Additionally, phosphorylation of JAK2, STAT3 and Akt was significantly enhanced both in IL-6/IL-6R-treated AAFs in vitro and in TAK adventitial α-SMA positive cells.
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.
Anti-tubulin-α-1c antibody levels were further determined by enzyme-linked immunosorbent assay (ELISA) in sera of patients with BD, systemic lupus erythematosus (SLE), recurrent aphthous ulcers (RAU), ANCA associated systemic vasculitis (AASV), Takayasu's arteritis (TA) and 59 healthy controls.
IL-6/IL-6R induces fibrogenesis of AAFs via the JAK2/STAT3 and JAK2/Akt pathways, which provides theoretical evidence for IL-6 as a treatment target in TAK.