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Year : 2019  |  Volume : 46  |  Issue : 4  |  Page : 262-268

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

1 Rheumatology Unit, Department of Internal Medicine, Faculty of Medicine, Alexandria University, Alexandria, Egypt
2 Department of Physical Medicine, Rheumatology and Rehabilitation, Faculty of Medicine, Alexandria University, Alexandria, Egypt
3 Department of Clinical and Chemical Pathology, Faculty of Medicine, Alexandria University, Alexandria, Egypt

Correspondence Address:
Rehab Elnemr
Lecturer, Department of Physical Medicine, Rheumatology and Rehabilitation, Faculty of Medicine, Alexandria University, Alexandria
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/err.err_14_19

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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.

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