MicroRNAs miR-17 and miR-20a Inhibit T Cell Activation Genes and Are Under-Expressed in MS Whole Blood
journal contributionposted on 2023-05-17, 03:24 authored by Cox, MB, Cairns, MJ, Gandhi, KS, Carroll, AP, Moscovis, S, Stewart, GJ, Broadley, S, Scott, RJ, Booth, DR, Lechner-Scott, J, Bahlo, M, Butzkueven, H, Brown, MA, Simon James FooteSimon James Foote, Griffiths, L, Kilpatrick, TJ, Moscato, P, Perreau, VM, Rubio, JP, Jim StankovichJim Stankovich, Bruce TaylorBruce Taylor, Wiley, J, Heard, RN
It is well established that Multiple Sclerosis (MS) is an immune mediated disease. Little is known about what drives the differential control of the immune system in MS patients compared to unaffected individuals. MicroRNAs (miRNAs) are small non-coding nucleic acids that are involved in the control of gene expression. Their potential role in T cell activation and neurodegenerative disease has recently been recognised and they are therefore excellent candidates for further studies in MS. We investigated the transcriptome of currently known miRNAs using miRNA microarray analysis in peripheral blood samples of 59 treatment naý¨ve MS patients and 37 controls. Of these 59, 18 had a primary progressive, 17 a secondary progressive and 24 a relapsing remitting disease course. In all MS subtypes miR-17 and miR-20a were significantly underexpressed in MS, confirmed by RT-PCR. We demonstrate that these miRNAs modulate T cell activation genes in a knock-in and knock-down T cell model. The same T cell activation genes are also up-regulated in MS whole blood mRNA, suggesting these miRNAs or their analogues may provide useful targets for new therapeutic approaches
Publication titleP L o S One
Department/SchoolMenzies Institute for Medical Research
PublisherPublic Library of Science
Place of publicationUnited States
Rights statementCopyright © 2010 Cox et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.