TCR-CD3ζ gene expression profile in patients with rheumatoid arthritis and correlation with disease activity

• Main Authors: Abeer Abdelati, Rehab Elnemr, Ahmed Ismail, Marwa Gamal-Eldeen
• Format: Article
• Language: English
• Published: SpringerOpen 2019-01-01
• Series: Egyptian Rheumatology and Rehabilitation
• Subjects: CD247; gene expression; PCR; rheumatoid arthritis; T-cell receptor-CD3 zeta chain
• Online Access: http://www.err.eg.net/article.asp?issn=1110-161X;year=2019;volume=46;issue=4;spage=262;epage=268;aulast=Abdelati
• ISSN: 1110-161X; 2090-3235

Objective To measure the T-cell receptor-CD3 zeta chain (TCR-CD3ζ) gene expression profile in a cohort of patients with rheumatoid arthritis (RA). Patients and methods A 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. Results TCR-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. Conclusion Our 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.