Acid Sphingomyelinase and Acid β-Glucosidase 1 Exert Opposite Effects on Interleukin-1β-Induced Interleukin 6 Production in Rheumatoid Arthritis Fibroblast-Like Synoviocytes.

Acid sphingomyelinase (ASM) and acid β-glucosidase 1 (GBA1) catalyze ceramide formation through different routes, and both are involved in rheumatoid arthritis (RA) pathogenesis as well as IL-6 production. However, whether ASM and GBA1 regulate IL-6 production in RA remains unknown. Serum ASM, GBA1, and ceramide levels were measured in RA patients and healthy controls by enzyme-linked immunosorbent assay, and their correlations with clinical indicators of patients were evaluated.

miR-431-5p regulates cell proliferation and apoptosis in fibroblast-like synoviocytes in rheumatoid arthritis by targeting XIAP.

Background: miR-431-5p is dysregulated in various cancers and plays an important function in the development of cancer. However, its role in fibroblast-like synoviocytes (FLSs) in patients with rheumatoid arthritis (RA) remains to be understood.

Methods: Quantitative real-time polymerase chain reaction was used to detect the relative expression of miR-431-5p in synovial tissues and FLSs.

LncRNA NEAT1 Targets Fibroblast-Like Synoviocytes in Rheumatoid Arthritis via the miR-410-3p/YY1 Axis.

LncRNA NEAT1 functions as an oncogene in multiple human cancers. However, its expression and role in fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA) remain unclear. Thus, we investigated the expression of NEAT1 in synovial tissues and FLSs in RA, to determine its role in the development of RA.

Pentraxin 3 inhibits fibroblast growth factor 2 induced osteoclastogenesis in rheumatoid arthritis.

Background: Synovial fibroblasts (SFs) act as key effector cells mediating synovial inflammation and joint destruction in rheumatoid arthritis (RA). Fibroblast growth factor 2 (FGF2) and its receptors (FGFRs) play important roles in RASF-mediated osteoclastogenesis. Pentraxin 3 (PTX3) is a soluble pattern recognition receptor with nonredundant roles in inflammation and innate immunity.

miR-483-3p promotes cell proliferation and suppresses apoptosis in rheumatoid arthritis fibroblast-like synoviocytes by targeting IGF-1.

Accumulating evidence suggests that miR-483-3p is implicated in maintaining biological properties in human cancers. However, its biological roles in rheumatoid arthritis (RA) remain unknown. miR-483-3p levels in synovial tissue samples and fibroblast-like synoviocytes (FLSs) were determined using quantitative real-time PCR.

Obesity promotes the global hypomethylation of CD4+ T cells in patients with systemic lupus erythematosus via downregulating DNMT1.

Background: The global hypomethylation of CD4 T cells in systemic lupus erythematosus (SLE) patients has been previously reported. However, potential influencing factors are unclear. This study aimed to uncover the potential influence of obese on hypomethylated CD4 T cells in SLE patients.

Meta-analysis of IL-17 inhibitors in two populations of rheumatoid arthritis patients: biologic-naïve or tumor necrosis factor inhibitor inadequate responders.

Objectives: To evaluate the efficacy and safety of interleukin 17 (IL-17) inhibitors in two rheumatoid arthritis (RA) populations: biologic-naïve or tumor necrosis factor inhibitor inadequate responders (TNF-IR).

Method: A systematic search was performed in major electronic databases to identify relevant randomized controlled trials (RCTs) reporting the American College of Rheumatology 20% (ACR20), ACR50, ACR70 responses and adverse events (AEs) of IL-17 inhibitors versus placebo in patients with RA. We divided these patients into two subgroups: biologic-naïve or TNF-IR.

Efficacy of anti-tumor necrosis factor therapy for extra-articular manifestations in patients with ankylosing spondylitis: a meta-analysis.

Background: We performed a meta-analysis to evaluate the effect of anti-tumor necrosis factor (TNF) therapy on the frequency of extra-articular manifestations (EAMs) in patients with ankylosing spondylitis (AS).

Methods: We searched with the terms 'ankylosing spondylitis', 'infliximab', 'etanercept', 'adalimumab', 'golimumab', 'certolizumab', 'TNF inhibitor/blocker/antagonists' or 'anti-TNF' on MEDLINE, EMBASE and Cochrane Library for randomized controlled trials (RCTs) of ≥ 12 weeks with parallel or crossover design of TNF inhibitor versus placebo to treat uveitis, inflammatory bowel disease (IBD) and/or psoriasis of AS, published before February 2014.

Results: We found 8 RCTs that fit our criteria.

Increased interleukin-23 is associated with increased disease activity in patients with rheumatoid arthritis.

Background: Interleukin-23 (IL-23) is a pro-inflammatory cytokine that is thought to be central to the development of autoimmune diseases. This study was conducted to determine whether or not the serum concentration of IL-23 is elevated in patients with rheumatoid arthritis (RA), and to determine the relationship between the IL-23 level and disease activity in RA patients.

Methods: Serum samples were obtained from 59 patients with RA and 30 healthy controls.

Effect of tumor necrosis factor inhibitors on rheumatoid arthritis-induced peripheral neuropathy: A cohort study.

In this historical cohort study, 236 patients with primary rheumatoid arthritis were treated with the tumor necrosis factor inhibitors, etanercept or infliximab (n = 80), or by conventional methods (n = 156). Results revealed that 11 patients developed varying types of peripheral neuropathy at 1-2 years post-treatment (mean 16 months). The incidence of peripheral neuropathy in the tumor necrosis factor inhibitors treatment group was 8.