Long intergenic noncoding RNA MIAT regulates human Th17 cell differentiation  and is highly expressed in T cells of inflamed synovia in joints of Rheumatoid Arthritis patients

    Long intergenic noncoding RNAs (lincRNA) are emerging as novel regulators of biological processes, including cell differentiation and development. While Th17 cells are required for clearing fungal and bacterial infections, dysregulation of Th17 response can result in autoimmunity such as rheumatoid arthritis.

    Researchers from Turku Bioscience identified Myocardial Infarction Associated Transcript (MIAT) lincRNA as a novel regulator of human Th17 cells.

    First demonstrating  that MIAT is significantly upregulated during early human Th17 cell differentiation they then showed that it is regulated by STAT3, a key transcription factor driving Th17 differentiation.

    • We found that MIAT is essential for Th17 differentiation; its silencing led to impaired Th17 specification and it positively regulated the expression of several Th17 signature genes, says Professor Riitta Lahesmaa, Director of Turku Bioscience and a group leader in the InFLAMES research flagship initiative.

    MIAT resides in the nucleus and appears to regulate the chromatin accessibility of key Th17 loci including IL17A locus.

    • Besides discovering MIAT to be functionally essential for Th17 differentiation we found MIAT to be upregulated in T cells of synovial biopsies from patients with rheumatoid arthritis, suggesting its role in the pathogenesis of this autoimmune disease and possibly other autoimmune disorders, says Professor Riitta Lahesmaa.

    The study was published in the Frontiers of Immunology. The study was funded by the Academy of Finland, The Sigrid Jusélius Foundation, the Jane & Aatos Erkko Foundation and InFLAMES Flagship.

    Khan MM, Khan MH, Kalim UU, Khan S, Junttila S, Paulin N, Kong L, Rasool O, Elo LL, Lahesmaa R. Long Intergenic Noncoding RNA MIAT as a Regulator of Human Th17 Cell Differentiation. Front Immunol. 2022 Jun 15;13:856762. doi: 10.3389/fimmu.2022.856762. eCollection 2022.

    More information: Riitta Lahesmaa, riitta.lahesmaa@utu.fi, tel. +358 40 718 4813