This study identifies a potentially important role for TNF-αrs1800629 polymorphisms in the susceptibility to RA.However, further studies in larger cohorts are required.
Variations in two genes of the tumour necrosis factor (TNF) alpha pathway have been implicated in the pathogenesis of autoimmune diseases: polymorphisms in the TNFRSF1A gene, encoding TNF receptor 1, showed significant association with MS in genomewide association scans, and variation in or near the TNFAIP3 gene, coding for a negative regulator of NFkB, was associated with MS, systemic lupus erythematosus, diabetes and rheumatoid arthritis.
Eighty-one patients with active RA were genotyped for the -308 TNFalpha polymorphism by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis and subdivided into two groups for each polymorphism (G/A and G/G genotype).
Mycobacterial diseases are prevalent in cancer and rheumatoid arthritis (RA) patients, especially those receiving tumor necrosis factor-α inhibitor (TNFi).
Accumulating evidences suggested that tumor necrosis factor alpha inducible protein 3 (TNFAIP3) gene rs10499194, rs13207033 polymorphisms may be associated with the risk of rheumatoid arthritis (RA).
We evaluated healthcare utilization before and after initiation of the tumor necrosis factor inhibitor etanercept in patients with moderate to severe RA.
No significant differences were observed either in the frequency of the TNF2 allele or in the genotypic distributions of the -308 G/ATNF-α polymorphism (P > 0.05) between the control group and the RA patients.
The aim of this study was to identify several specific reliable metabolites for predicting the response of RA patients to TNF-α inhibitors (TNFi) and abatacept (ABT), using capillary electrophoresis-time-of-flight mass spectrometry (CE-TOFMS).
In this study, we investigated the differential pattern of distribution of TNF microsatellite alleles in an Indian population and its association with RA.
We aimed to test whether polymorphisms in the etanercept target genes TNFA and LTA are associated with clinical responses to etanercept therapy in RA patients.
Patients with rheumatoid arthritis (RA) can be successfully treated with tumor necrosis factor (TNF) inhibitors, including the monoclonal antibody adalimumab.
Tocilizumab 8 mg combined with MTX or as monotherapy was the most effective treatment for active RA with an inadequate MTX or TNF antagonist response, followed by sarilumab and sirukumab, regardless of MTX combination.
Our results indicated that IL-1RN VNTR, IL-1β (-511C>T) and IL-10 (-1082 G>A) are associated with susceptibility to RA, and that IL-1RN VNTR, IL-1β (-511C>T) and TNFα (-308 G>A) are associated with severity of RA.
In an RA population from NW Spain the frequencies of HLA-DRB1 and TNF microsatellite alleles in patients with extra-articular manifestations were not significantly different to those without extraarticular disease, although there was a trend towards increased frequency of HLA-DRB1*0101 in patients with nodular disease.
The aim of this study was to investigate the incidence of invasive cutaneous melanomas in patients with rheumatoid arthritis (RA) treated with TNF inhibitors (TNFi), other biologic disease modifying drugs and non-biologic therapy.
We performed a systematic review and meta-analysis to evaluate the comparative effects of tumor necrosis factor-α inhibitors (TNFi), non-TNFi biologic and conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs) on cardiovascular risk in rheumatoid arthritis (RA).
In this regard, besides a strong association between the HLA-DRB1∗04 shared epitope alleles and both endothelial dysfunction, an early step in the atherosclerotic process, and clinically evident CV disease, other polymorphisms belonging to genes implicated in inflammatory and metabolic pathways, located inside and outside the HLA region, such as the 308 variant (G > A, rs1800629) of the TNFA locus, the rs1801131 polymorphism (A > C; position + 1298) of the MTHFR locus, or a deletion of 32 base pairs on the CCR5 gene, seem to be associated with the risk of CV disease in patients with RA.
The presence of rheumatoid factor and anti-cyclic citullinated protein antibodies, present in around 65% of RA patients, are associated with a poorer response to anti-TNF agents.
Interaction between tumor necrosis factor microsatellite polymorphisms and the HLA-DRB1 shared epitope in rheumatoid arthritis: influence on disease outcome.
Using an activity-impaired sPLA(2)-IIA mutant protein (H48Q), we show that up-regulation of TNF-dependent PGE(2) production and cyclooxygenase-2 (COX-2) induction by exogenous sPLA(2)-IIA in RA fibroblast-like synoviocytes (FLSs) is independent of its enzyme function.