However, Midkine presents a significantly higher diagnostic accuracy (AUC=0.939) in detecting RA activity than that offered by C reactive protein (CRP) or ESR.
In the full cohort and in RA, baseline and/or 12-month bone mineral density (BMD) at multiple sites exerted inverse relationships with CRP and βCTX, and positive correlation with SOST.
Live birth deliveries were significantly protective for women with 0 but not for those with 1 or 2 copies of the RA risk-associated HLA-DRB1 shared epitope sequence for erosion score (RR 0.26 95% CI 0.09-0.89) and joint count (RR 0.28 95% CI 0.09-0.87).
<b>Conclusion</b>: Serum capacity to activate PAD4 was associated with ACPA and RF positivity and earlier disease onset in early RA patients, and decreased after initiation of DMARD treatment, indicating that anti-PAD treatment could potentially be beneficial in RA.
This study evaluated the possible association between SNPs in cytokines coding genes, namely IL10, IL6 and IFNG, cytokines serum levels and clinical assessment' scores in patients with Rheumatoid Arthritis(RA).
In conclusion, our study demonstrates a functional effect of <i>IL12B</i> polymorphisms on IL-12p40 and IL-23 cytokine levels in RA patients and suggests a leading role for <i>IL12B</i> rs17860508 in the genetic predisposition to RA, while <i>IL12B</i> rs3212227 significantly modify the RA risk in Bulgarian population.
Notably, the Pearson coefficient demonstrated that the levels of the RAS components were positively correlated with the expression of VEGF and MMP-13 in OA and RA.
The aim of the present study was to evaluate the effects of rapamycin, under the generic name sirolimus, on CD4+CD25+FoxP3+ Treg cells in rheumatoid arthritis (RA) patients with low disease activity or in DAS28 remission.
To date, the therapeutic armamentarium for RA includes ten bDMARDs able to produce the depletion B-cells, the blockade of three different pro-inflammatory cytokines (tumour necrosis factor alpha, interleukin-6 and interleukin-1), or the inhibition of T-cell co-stimulation.
This study evaluated the possible association between SNPs in cytokines coding genes, namely IL10, IL6 and IFNG, cytokines serum levels and clinical assessment' scores in patients with Rheumatoid Arthritis(RA).
The aim of this study was to evaluate the association of MIF promoter polymorphisms (-794CATT<sub>5-8</sub> rs5844572 and -173G > C, rs755622), circulating MIF levels, and mRNA expression with RA susceptibility and disease activity.
Furthermore, other reported AhR antagonists also upregulate utrophin, showing that this pathway, which is currently being explored in other clinical applications including oncology and rheumatoid arthritis, could also be exploited in future DMD therapies.
Furthermore, both TNF-α and IL-6 are important pathogenic factors related to immune-mediated bone diseases including rheumatoid arthritis and postmenopausal osteoporosis.
TNFR2 associates with FoxP3 stability and identifies asubset of regulatory T cells that are specifically expanded by anti-TNF treatments in rheumatoid arthritis.
These findings collectively implicated an important role of IL-6 in driving PTX3 plus C1q-mediated pyroptosis in RA and shed lights on a potential new treatment strategy targeting pyroptosis-mediated persistent inflammatory cytokine release.
This study aimed to evaluate the combinatorial effect of TNF and IL-6 inhibitors on the differentiation and activation of Th17 cells and osteoclasts in the context of RA, and to identify the RA-related mechanisms through IL-6 signaling.
Neutrophils and peripheral blood mononuclear cells (PBMCs) were isolated from three patients diagnosed with RA and treated with various concentrations of IGU, methotrexate (MTX), or dexamethasone (DXM) or without any drugs as a control for 8 h. The levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8 in culture supernatants were tested by ELISA.