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.
Gene-environment associations are important in rheumatoid arthritis (RA) susceptibility, with an association existing between smoking, HLA- DRB1 'shared epitope' alleles, PTPN22 and antibodies to cyclic citrullinated peptides (CCP).
In contrast with a study of American patients with RAno evidence of association with PTPN22 independent of the well-characterised R620W variant was found, suggesting that in these patients this variant alone explains the association with the PTPN22 gene.
The autoimmune-associated genetic variant PTPN22R620W enhances neutrophil activation and function in patients with rheumatoid arthritis and healthy individuals.
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).
A functional variant of protein tyrosine phosphatase nonreceptor 22 (PTPN22) has recently been shown to be associated with multiple autoimmune diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis, type 1 diabetes, and autoimmune thyroid disease.
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.
PTPN22 polymorphism and anti-cyclic citrullinated peptide antibodies in combination strongly predicts future onset of rheumatoid arthritis and has a specificity of 100% for the disease.
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.
ORs for associations with different HLA-DRB1 alleles, PTPN22 genotypes and smoking were calculated separately for each cohort as well as in meta-analysis in RA subsets defined by the presence/absence of anti-CarP and anticyclic citrullinated peptide (anti-CCP) antibodies.
Interactions between HLA and PTPN22 genotypes and smoking have been implicated in overall susceptibility to rheumatoid arthritis as well as the incidence of particular disease phenotypes in case-control and case-only studies.
The PTPN22 variant was strongly associated with T1D in cases vs controls (P=2 x 10(-7), OR=2.3, 95% CI=1.7-3.1) as well as in a transmission disequilibrium test in nuclear trio's (P=9 x 10(-9), OR=3.3, CI=2.1-5.0), RA (case/control: P=0.003, OR=1.8 CI =1.2-2.6), but not CD, in spite of a trend of increased homozygosity (P=0.05) and early age at onset (P=0.01).