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The Putative Association of TOB1-AS1 Long Non-coding RNA with Immune Tolerance: A Study on Multiple Sclerosis Patients

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Abstract

The hallmark of multiple sclerosis (MS) pathogenesis is the breakdown of peripheral tolerance in the immune system. However, its molecular mechanism is not completely understood. Since long non-coding RNAs (lncRNAs) has played important roles in regulation of immunological pathways, here, we evaluated the expression of a novel lncRNA, TOB1-AS1, and its putative associated coding genes in the mechanism of maintaining immune tolerance in peripheral blood of MS patients to assess their possible roles in MS pathogenesis. In this study, 39 MS patients and 32 healthy matched controls were recruited. Real-time PCR standard curve method was used to quantify transcript levels of TOB1-AS1, TOB1, SKP2, and TSG. In addition, the potential sex hormone receptor binding sites on target genes promoter were analyzed using JASPR software. This work demonstrates a negative correlation between TOB1-AS1 expression and EDSS of patients. Also, a robust dysregulation of co-expression of TOB1-AS1 lncRNA and the coding genes in MS patients compared to controls was observed. Such dysregulation in this pathway may be related to MS pathogenesis and response to interferon treatment.

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Acknowledgements

The authors gratefully acknowledge the contribution of the patients and controls for their participation in this study.

Funding

This work is supported by the Iran National Science Foundation and the Department of research Affairs of Tarbiat Modares University.

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Correspondence to Mehrdad Behmanesh.

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All procedures performed in studies involving human participants were in accordance with the ethics committee of Tarbiat Modares University and with the 1964 Helsinki Declaration.

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Dehghanzad, R., Pahlevan Kakhki, M., Alikhah, A. et al. The Putative Association of TOB1-AS1 Long Non-coding RNA with Immune Tolerance: A Study on Multiple Sclerosis Patients. Neuromol Med 22, 100–110 (2020). https://doi.org/10.1007/s12017-019-08567-1

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