The effect of TGF-β1 gene expression on patients with rheumatoid arthritis
Abstract
Background: A systemic autoimmune disease, rheumatoid arthritis (RA), affects a wide range of ages and populations worldwide. In chronic RA, lymphocytes, synovial cells, antigen-presenting cells, their cytokines, and most importantly, Transforming Growth Factor-β1 (TGF-β1) are the leading players. The most critical for angiogenesis, immunosuppression, fibrosis, and chronic inflammation is TGF-β1, a potent anti-inflammatory mediator in RA with high expression at the site of RA.
Methods: A total of 53 rheumatoid arthritis (RA) patients (anti-CCP and RF positive) and 18 age- and sex-matched healthy controls were recruited using purposive sampling. Patients were enrolled from Al Zahraa Hospital, Al Karama Teaching Hospital, and affiliated clinics in Wasit Province. Inclusion criteria comprised confirmed RA diagnosis according to ACR/EULAR 2010 criteria, while patients with other autoimmune, infectious, or chronic inflammatory diseases were excluded. Ethical approval was obtained from the institutional review board, and informed consent was secured from all participants. Blood samples were collected for TGF-β1 gene expression analysis using RT-qPCR. Erythrocyte sedimentation rate (ESR) was determined, and disease activity was classified using the DAS28 score.
Results: RA patients showed significantly higher TGF-β1 expression than controls (ΔΔCt = −0.9 ± 2; t(52) = −3.28, P = 0.0019), corresponding to a geometric mean fold change of 1.87 [95 % CI: 1.28 – 2.71]. The expression of TGF-β1 on leukocytes did not vary significantly between males and females. Furthermore, TGF-β1 gene expression did not change amongst patients with low, moderate, and high disease activity levels.
Conclusion: The elevated level of TGF-β1 in the contemporary study might be correlated with RA in Iraqi patients. This relationship seems independent of gender and disease activity status and highlights the importance of TGF-β1 in RA pathogenesis, indicating its possible contribution as a disease detection biomarker. The implications of these findings are significant for understanding the molecular mechanisms underlying RA and may influence future therapeutic strategies.
Keywords: Rheumatoid arthritis, TGF-β1, Expression, Cytokines, Autoimmune disease
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DOI: http://dx.doi.org/10.62940/als.v12i3.2019
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