Hyppää sisältöön
    • Suomeksi
    • In English
  • Suomeksi
  • In English
  • Kirjaudu
Näytä aineisto 
  •   Etusivu
  • 3. UTUCris-artikkelit
  • Rinnakkaistallenteet
  • Näytä aineisto
  •   Etusivu
  • 3. UTUCris-artikkelit
  • Rinnakkaistallenteet
  • Näytä aineisto
JavaScript is disabled for your browser. Some features of this site may not work without it.

Long Intergenic Noncoding RNA MIAT as a Regulator of Human Th17 Cell Differentiation

Lahesmaa Riitta; Junttila Sini; Kalim Ubaid Ullah; Khan Meraj Hasan; Elo Laura L; Rasool Omid; Paulin Niklas; Khan Sofia; Kong Lingjia; Khan Mohd Moin

Long Intergenic Noncoding RNA MIAT as a Regulator of Human Th17 Cell Differentiation

Lahesmaa Riitta
Junttila Sini
Kalim Ubaid Ullah
Khan Meraj Hasan
Elo Laura L
Rasool Omid
Paulin Niklas
Khan Sofia
Kong Lingjia
Khan Mohd Moin
Katso/Avaa
fimmu-13-856762.pdf (5.648Mb)
Lataukset: 

FRONTIERS MEDIA SA
doi:10.3389/fimmu.2022.856762
URI
https://www.frontiersin.org/articles/10.3389/fimmu.2022.856762/full
Näytä kaikki kuvailutiedot
Julkaisun pysyvä osoite on:
https://urn.fi/URN:NBN:fi-fe2022091258436
Tiivistelmä
T helper 17 (Th17) cells protect against fungal and bacterial infections and are implicated in autoimmunity. Several long intergenic noncoding RNAs (lincRNA) are induced during Th17 differentiation, however, their contribution to Th17 differentiation is poorly understood. We aimed to characterize the function of the lincRNA Myocardial Infarction Associated Transcript (MIAT) during early human Th17 cell differentiation. We found MIAT to be upregulated early after induction of human Th17 cell differentiation along with an increase in the chromatin accessibility at the gene locus. STAT3, a key regulator of Th17 differentiation, directly bound to the MIAT promoter and induced its expression during the early stages of Th17 cell differentiation. MIAT resides in the nucleus and regulates the expression of several key Th17 genes, including IL17A, IL17F, CCR6 and CXCL13, possibly by altering the chromatin accessibility of key loci, including IL17A locus. Further, MIAT regulates the expression of protein kinase C alpha (PKC alpha), an upstream regulator of IL17A. A reanalysis of published single-cell RNA-seq data showed that MIAT was expressed in T cells from the synovium of RA patients. Our results demonstrate that MIAT contributes to human Th17 differentiation by upregulating several genes implicated in Th17 differentiation. High MIAT expression in T cells of RA patient synovia suggests a possible role of MIAT in Th17 mediated autoimmune pathologies.
Kokoelmat
  • Rinnakkaistallenteet [19207]

Turun yliopiston kirjasto | Turun yliopisto
julkaisut@utu.fi | Tietosuoja | Saavutettavuusseloste
 

 

Tämä kokoelma

JulkaisuajatTekijätNimekkeetAsiasanatTiedekuntaLaitosOppiaineYhteisöt ja kokoelmat

Omat tiedot

Kirjaudu sisäänRekisteröidy

Turun yliopiston kirjasto | Turun yliopisto
julkaisut@utu.fi | Tietosuoja | Saavutettavuusseloste