Whole-Exome Sequencing and Analysis of the T Cell Receptor ß and γ Repertoires in Rheumatoid Arthritis.

This study investigated the potential genetic variants of rheumatoid arthritis (RA) using whole-exome sequencing (WES) and evaluated the disease course using T cell receptor (TCR) repertoire analysis. Fourteen patients with RA and five healthy controls (HCs) were enrolled. For the RA patient group, only treatment-naïve patients were recruited, and data were collected at baseline as well as at 6 and 12 months following the initiation of the disease-modifying antirheumatic drug (DMARD) treatment. Laboratory data and disease parameters were also collected. Genetic variants were detected using WES, and the diversity of the TCR repertoire was assessed using the Shannon-Wiener diversity index. While some variants were detected by WES, their clinical significance should be confirmed by further studies. The diversity of the TCR repertoire in the RA group was lower than that in the HCs; however, after DMARD treatment, it increased significantly. The diversity was negatively correlated with the laboratory findings and disease measures with statistical significance. Variants with a potential for RA pathogenesis were identified, and the clinical significance of the TCR repertoire was evaluated in Korean patients with RA. Further studies are required to confirm the findings of the present study.

Adipokines, inflammation, insulin resistance, and carotid atherosclerosis in patients with rheumatoid arthritis.

INTRODUCTION: Cardiovascular (CV) morbidity and mortality are increased in patients with rheumatoid arthritis (RA). Inflammation is thought to be an important factor in accelerated atherosclerosis in RA, whereas insulin resistance is a known risk factor for atherosclerosis in RA. We hypothesised that adipokines could be a link between inflammation, insulin resistance, and atherosclerosis in RA. METHODS: The common carotid artery (CCA) intima-media thickness (IMT), CCA resistive index (RI), and carotid plaques were measured by ultrasonography in 192 patients with RA. Insulin resistance was assessed by the homeostasis model assessment for insulin resistance (HOMA-IR). Serum adiponectin, leptin, resistin, tumor necrosis factor-α, and interleukin (IL)-6 concentrations were determined. RESULTS: The CCA RI was associated with CCA IMT and the estimated total plaque volume after adjustment for conventional CV risk factors. Among adipokines, resistin and IL-6 were correlated with inflammatory parameters. Leptin and leptin:adiponectin (L:A) ratio were correlated with metabolic risk factors, including HOMA-IR. And L:A ratio was related to the CCA RI after adjustment for conventional and nonconventional CV risk factors, including HOMA-IR, erythrocyte sedimentation rate and C-reactive protein. CONCLUSION: L:A ratio was associated with HOMA-IR and carotid RI. L:A ratio might be an independent factor for predicting cardiovascular risk in patients with RA.