Association analysis among DMA, DMB, and DRB1*1502 in Japanese SSc with diffuse scleroderma and SSc with a-Scl-70 indicated that the increase in DMA*0101 was not primary, but reflected an increase in HLA DRB1*1502.
Here, we report of rebound reaction in the gene expression of melanocortin receptor (MCR) subtypes and of the precursor of these receptors' ligands, the pro-opio-melanocortin protein (POMC), in the acute skin lesion of diffuse systemic sclerosis (dSSc) after treatment with a recombinant human anti-TGFβ1 antibody.
To explore the expression of thymic stromal lymphopoietin (TSLP) in patients with diffuse cutaneous systemic sclerosis (dcSSc) and compare its effects in vivo and in vitro with those of interleukin-13 (IL-13) and transforming growth factor β (TGFβ).
BANK1 haplotype analysis found the A-T haplotype to be protective in dcSSc patients (OR 0.70 [95% CI 0.57-0.86], P = 3.39 x 10(-4)) and the G-C haplotype to be a risk factor (OR 1.25 [95% CI 1.06-1.47], P = 0.008).
In addition, DRB1*0802 was also increased in DRB1*1502 negative patients with a-Scl-70, (50.0%, p = 0.033, pc = not significant) and in DRB1*1502 negative patients with diffuse scleroderma (75.0%, p = 0.008, pc = not significant).
To evaluate CAT-192, a recombinant human antibody that neutralizes transforming growth factor beta1 (TGFbeta1), in the treatment of early-stage diffuse cutaneous systemic sclerosis (dcSSc).
This dataset showed tumor necrosis factor-α, IFN-γ, transforming growth factor-β, and IL-13 as potential upstream regulators of the serum protein patterns in the sera of patients with diffuse cutaneous systemic sclerosis.
Scleroderma (progressive systemic sclerosis; PSS) is a connective tissue disorder in which excessive collagen is deposited in the skin and internal organs.
Simultaneous inhibition of c-Abl and Src kinases with Bosutinib abrogates the exaggerated expression of genes encoding fibrillar collagens, fibronectin, and TGF-β-responsive genes and reduces type I collagen, fibronectin and α-SMA production by SSc dermal fibroblasts in vitro.
Association analysis among DMA, DMB, and DRB1*1502 in Japanese SSc with diffuse scleroderma and SSc with a-Scl-70 indicated that the increase in DMA*0101 was not primary, but reflected an increase in HLA DRB1*1502.
Epidermal growth factor receptor (EGF-R) of fibroblasts from 3 patients with scleroderma (progressive systemic sclerosis, PSS) was studied by radioiodinated-EGF binding assay.
This study intends to analyze the genetic correlation of the ctla-4 gene locus with diffuse systemic sclerosis (dSSc), as well as to understand the influence of these genotypes in disease expression.
Cytoplasmic autoantibodies (in otherwise ANA-negative sera) targeting eukaryotic initiation factor-2B (anti-eIF2B) have recently been identified in SSc with clinical associations to dcSSc disease and interstitial lung disease (ILD), although the majority of samples originated from a tertiary SSc-ILD centre.
Association analysis among DMA, DMB, and DRB1*1502 in Japanese SSc with diffuse scleroderma and SSc with a-Scl-70 indicated that the increase in DMA*0101 was not primary, but reflected an increase in HLA DRB1*1502.
The frequency of non-classical monocytes spontaneously producing CXCL10 was increased in both limited (lcSSc) and diffuse cutaneous (dcSSC) subsets of SSc patients and CCL4 was augmented in dcSSc patients.
We evaluated patients from the European Scleroderma Trials and Research database with dcSSc, baseline modified Rodnan skin score (mRSS) ≥7, valid mRSS at 12±3 months after baseline and ≥1 annual follow-up visit.
The data also indicate that first-intron sequences of COL1A1 are required for maximal transcriptional activity of the collagen gene and may play an important role in the up-regulation of its expression in SSc fibroblasts.