Abstract
ObjectiveTo measure the T-cell receptor-CD3 zeta chain (TCR-CD3ζ) gene expression profile in a cohort of patients with rheumatoid arthritis (RA).Patients and methodsA case—control study on 150 consecutive RA patients diagnosed according to 2010 ACR/EULAR criteria and 150 matched healthy controls without a family history of RA or other autoimmune diseases. RA patients with other autoimmune diseases, viral hepatitis B or C, malignancy or hematological disorders were excluded from the study. All participants were subjected to history taking, clinical examination, assessment of disease activity (in RA patients) using Disease Activity Score-28 and Health Assessment Questionnaire, routine laboratory investigations, inflammatory marker levels, serological tests, as well as molecular analysis for TCR-CD3ζ mRNA expression by quantitative real-time PCR.ResultsTCR-CD3ζ gene expression was significantly lower in RA cases than in controls (P<0.05). Expression of TCR-CD3ζ has shown a significant negative correlation with RA disease duration, rheumatoid factor, and erythrocyte sedimentation rate (P<0.05) in RA cases. The level of TCR-CD3ζ also showed a significantly less expression in patients with positive rheumatoid factor.ConclusionOur results demonstrated a lower expression of TCR-CD3ζ in RA patients than in healthy controls. We suggested that CD247 gene downregulation might contribute in the susceptibility to RA and help understanding the pathways responsible for deficient T-cell responses in RA patients.
Highlights
Rheumatoid arthritis (RA) is the most common systemic inflammatory disease with articular and extra-articular manifestations [1,2]
This study was conducted on 150 RA patients (117 women and 33 men) with a mean age of 30.04±10.26 years (RA cases), and 150 (123 women and 27 men) healthy controls (HC) with a mean age of 35.14±9.12 years
Since changes in the CD3ζ chain may affect negatively the internal signaling cascade of the T-cell receptor (TCR) and lead to defective T-cell activation, our observations suggested that CD247 gene downregulation in our cohort of RA cases may contribute in the susceptibility to RA and help comprehending the mechanisms that may lead to deficient T-cell responses in RA patients as well as this downregulation is correlated with disease activity and functional status
Summary
Rheumatoid arthritis (RA) is the most common systemic inflammatory disease with articular and extra-articular manifestations [1,2]. It affects 1–2% of the population worldwide, with women affected 2–3 times more commonly than men [3]. Many studies identified genetic loci linked to RA such as HLA-DRB1 [5] and cytotoxic T-lymphocyte protein 4 [6]. The initiation and progression of the inflammatory disorder is controlled through the activation and signaling of specific cell surface chemoattractant receptors by their cognate protein ligands, termed chemokines [7]
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