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Regarding our manuscript: Tim-3-immune checkpoint receptor expression on CD4+ and CD8+ T cells and rheumatoid arthritis disease activity

Article scientifique 2022 Anglais

Résumé

Abstract Background Rheumatoid arthritis (RA), is a chronic inflammatory autoimmune disease, characterized by dysregulated T cell immune response.. Objective To investigate the Tim-3 surface expression on peripheral blood CD4+ and CD8+ T cells in RA patients concerning disease activity. Methods A cross-sectional case-controlled study involving 157 RA patients who were categorized by disease activity score 28 (DAS28) into 4 groups; patients with remission and low, moderate, and high RA activity groups. The assessment of Tim-3 expression on peripheral CD4 and CD8 T cells of patients and controls using flow cytometry was done. Results The peripheral expression of Tim-3 on CD4 + and CD8 + T cells was significantly higher in RA patients as compared to controls (for CD4 + T cells, 3.55 ± 1.12% in remission group vs. 1.21 ± 0.52 in control group, p < 0.001; for CD8 + T cells, 5.95 ± 1.49% in remission group vs. 1.80 ± 0.73% in control group, p < 0.001). There was an inverse correlation between percentages of both peripheral Tim-3 + CD4 + and Tim-3 + CD8 + T cell and RA DAS28, (r = − 0.425, p = 0.001) and (r= − 0.597, p = < 0.001) respectively. Conclusion The upregulated Tim-3 expression on peripheral CD4 + and CD8 + T-cells suggests a potential role of this immune checkpoint receptor in T cell immune dysregulation in RA. Tim-3 expression was negatively correlated with disease progression. Tim-3 could be a useful biomarker in determining the rheumatoid disease activity, progression, and represents an important target for inhibitors intervention in RA.

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Soliman, T., Abualfadl, E., Radwan, A., Amrosy, Y., El-kannishy, S., Elmansoury, E., Aboelnour, A., Ahmed, H. (2022). Regarding our manuscript: Tim-3-immune checkpoint receptor expression on CD4+ and CD8+ T cells and rheumatoid arthritis disease activity. https://doi.org/10.21203/rs.3.rs-1499145/v1

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