T-lymphocyte subsets (CD3+, CD4+, and CD8+) in Systemic Lupus Erythematosus (SLE): Correlation with Clinical Manifestation

Document Type : Original Article

Authors

1 Zoology Department, Faculty of Science, Menoufia University, Shebin El-Kom 32511, Menoufia, Egypt

2 Molecular Biology Department, Genetic Engineering and Biotechnology Research Institute (GEBRI), University of Sadat City, Egypt

3 Rheumatology and Rehabilitation Department, Faculty of Medicine, Cairo University, Cairo, Egypt

Abstract

AIM: Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that has a multifactorial etiology. T- Lymphocytes are essential in SLE pathogenesis. It plays a crucial role in autoantibody production and the subsequent immune complex formation, which may induce or directly damage multiple organs. This study was carried out aiming to quantify certain T lymphocyte subsets (CD3+, CD4+, and CD8+) in SLE patients and to elucidate if there is a possible influence of disease activity scores and clinical manifestations. Patients and Methods: This study included 100 SLE patients with various disease activity scores (SLEDAI) and 100 healthy age and sex-matched controls. The frequency of CD3+, CD4+, and CD8+ was assessed by flow cytometry. Results: A significant up-regulation in CD3+ (P<0.01), CD8+ (P<0.001) coincides with a significant downregulation in CD4+cells (P<0.001) were detected in SLE patients compared to controls. A significant up-regulation in CD4+ (P<0.05) was demonstrated in active SLE patients compared with the inactive form of the disease. On the other hand, no significant change was observed in the frequency of CD3+ and CD8+T cell subsets between active and inactive patients. Arthritic patients have a significant reduction in CD3+ and CD4+ T cells while those with Vasculities significantly reduce in CD4+, CD8+ compared with SLE patients without these manifestations.   Conclusion: The current study results stressed the importance of T cell subsets in SLE disease. They might participate in disease activity and in controlling several manifestations of lupus. Our findings will help design more studies on the role of T cell subsets in SLE pathogenesis which may provide new therapeutic targets for SLE.

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