miR-155 and functional proteins of CD8+ T cells as potential prognostic biomarkers for relapsing-remitting multiple sclerosis

Mult Scler Relat Disord. 2021 Jun 11;53:103078. doi: 10.1016/j.msard.2021.103078. Online ahead of print.


BACKGROUND: Multiple Sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) that results in neurological deficits in patients leading to disabilities which are evaluated on a scale known as the Expanded Disability Status Scale (EDSS). The most prevalent subtype of the disease is Relapsing-Remitting Multiple sclerosis (RRMS). One of the key players in MS pathogenesis is CD8+ T cells present in abundance in MS lesions expressing surface receptors, intracellular adhesion molecule (ICAM1) and integrin Subunit Beta 2 (ITGB2). These proteins are crucial for migration through the blood-brain barrier (BBB) and secondary stimulatory signal, along with the cytotoxic proteins perforin and granzymeB that attack oligodendrocytes. MicroRNAs (miRNAs) are small non-coding RNAs that play a substantial regulatory role in various disease pathogeneses through post-transcriptional modifications, and miR-155 shows potential for its use as a biomarker of the disease. The study aims at investigating the expression of miR-155, ICAM1, ITGB2, perforin and GranzymeB in CD8+ T cells of RRMS patients receiving different treatment regimens and how these genes correlate with patients’ EDSS and miR-155 expression.

METHODS: Gene expression of miR-155, ICAM1, ITGB2, perforin and granzymeB was evaluated using RT-qPCR in CD8+ T cells isolated from blood samples of RRMS patients and compared to healthy controls.

RESULTS: Results showed downregulation of miR-155 and upregulation of surface receptors and cytotoxic proteins in CD8+T cells with significant correlation with each other and patients’ EDSS.

CONCLUSION: This study helps pave the road for the discussed genes for their use as potential biomarkers of disease disability and future investigations on their regulatory roles in disease pathogenesis.

PMID:34171684 | DOI:10.1016/j.msard.2021.103078