CCR9 + T helper (Th) cells can induce Sjögren-like symptoms in mice and both CCR9 + Th cells and their ligand CCL25 are increased in the salivary glands of primary Sjögren's syndrome (pSS) patients.
Citrullinated vimentin and biglycan protein fingerprints as candidate serological biomarkers for disease activity in systemic sclerosis: a pilot study.
Treatment with exogenous factors, gelatin-1, FAM20A and human albumin, which were identified from the conditioned medium of SSc fibroblasts, was important for regulating the differentiation of fibroblasts with higher levels of SOCE and α-SMA.
A total of 26 of these miRNAs targeted genes involved in pathways connected to the three main features of SSc and to cancer development including Epidermal growth factor (EGF) receptor, ErbB1 downstream, Sphingosine 1 phosphate receptor 1 (S1P1), Activin receptor-like kinase 1 (ALK1), Endothelins, Ras homolog family member A (RhoA), Class I Phosphoinositide 3-kinase (PI3K), mammalian target of rapamycin (mTOR), p38 mitogen-activated protein kinase (MAPK), Ras-related C3 botulinum toxin substrate 1 (RAC1), Transforming growth factor (TGF)-beta receptor, Myeloid differentiation primary response 88 (MyD88) and Toll-like receptors (TLRs) pathways.
In a mouse model of bleomycin-induced fibrosis (n = 5-8) and in a TSK mouse model (a genetic model of SSc) (n = 5-10), deficient expression of MFG-E8 significantly enhanced both pulmonary and skin fibrosis, and administration of rMFG-E8 significantly inhibited bleomycin-induced dermal fibrosis.
Association of NCF1 polymorphism with systemic lupus erythematosus and systemic sclerosis but not with ANCA-associated vasculitis in a Japanese population.
Serum concentrations of Ang1 were significantly lower [mean (S.D.): 21516.04 (11,441.035) pg/ml], and Ang2 significantly increased [25,89.55 (934.225) pg/ml] in SSc as compared with the control group [Ang1: 28,457.08 (10,431.905) pg/ml; Ang2: 1556.23 (481.255) pg/ml, p < 0.01, respectively], whereas VEGF did not differ significantly.
In subgroup analysis, patients with higher modified Rodnan skin score (mRodnan) had higher DKK-1, sclerostin, and TRAIL levels (<i>p</i> < 0.05); those with diffuse SSc subtype had lower BMD values than those with limited SSc (<i>p</i> < 0.05).
Emerging diversity and abundance of the innate signature in RA patients were detected: RA was characterized by the upregulation of <i>TLR3</i>, <i>TLR5</i>, <i>IL1RAP/IL1R3</i>, <i>IL18R1</i>, and <i>SIGIRR/IL1R8</i> when compared to SSc (<i>P</i><sub>corr</sub> < 0.02) and of <i>TLR2</i>, <i>TLR5</i>, and <i>SIGIRR/IL1R8</i> when compared to SLE (<i>P</i><sub>corr</sub> < 0.02).
Moreover, we demonstrated that the hsa-miR-26b-5p inhibitor might inhibit fibrosis in TGF-β-activated fibroblasts, which would be a promising target for SSc therapy.
The purpose of this study was to investigate whether single nucleotide polymorphisms (SNPs) of TLR2, TLR3, TLR4 and TLR9 genes are associated with susceptibility to presumed viral-induced anterior uveitis (PVIAU) and Posner-Schlossman syndrome (PSS).
There was no significant difference between SSc patients and controls regarding either PI or MFV of the anterior, middle, and posterior cerebral arteries; also, there was no difference regarding the third ventricle diameter; however, limited SSc patients showed a significant increase in the PI of PCA and MFV of ACA as compared with diffuse SSc patients (p = 0.005, 0.004).
Remarkably, induction of CXCL10 and CXCL11, two IFN-related chemokines associated with SSc pathogenesis, was reduced in NRIR-knockdown monocytes, while their plasmatic level was increased in SSc patients.
Applying the association rule analysis, six rules (combinations and expression of genes describing disease) were identified for RA (most frequently included high <i>TLR3</i> and/or <i>IL1RAP/IL1R3</i>) and three rules for SLE (low <i>IL1RN</i> and <i>IL18R1</i>) and SSc (low <i>TLR5</i> and <i>IL18R1</i>).