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Enhanced STAT3 phosphorylation and PD-L1 expression in myeloid dendritic cells indicate impaired IL-27Ralpha signaling in type 1 diabetes
Z. Parackova, P. Vrabcova, I. Zentsova, J. Kayserova, I. Richtrova, L. Sojka, K. Stechova, Z. Sumnik, A. Sediva,
Jazyk angličtina Země Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NV16-32838A
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
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- MeSH
- antigeny CD274 genetika metabolismus MeSH
- dendritické buňky imunologie MeSH
- diabetes mellitus 1. typu genetika imunologie metabolismus MeSH
- dospělí MeSH
- fosforylace MeSH
- interleukiny genetika metabolismus MeSH
- lidé středního věku MeSH
- lidé MeSH
- receptory interleukinů genetika metabolismus MeSH
- sekvenční analýza hybridizací s uspořádaným souborem oligonukleotidů MeSH
- senioři MeSH
- signální transdukce * MeSH
- stanovení celkové genové exprese metody MeSH
- studie případů a kontrol MeSH
- transkripční faktor STAT3 metabolismus MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Interleukin 27 (IL-27), a member of the IL-12 family, is important for T cell differentiation; however, little is known about its effect on dendritic cells (DCs). IL-27 can activate multiple signaling cascades, including the JAK/STAT pathway, and depending on the setting it can both promote and antagonize inflammatory responses. An anti-inflammatory function of IL-27 has been reported in several autoimmune diseases; however, in type 1 diabetes (T1D), an autoimmune disease where autoreactive cytotoxic T cells attack insulin-producing beta cells, IL-27 has been shown to have a dual role and contradictory effects. Here, we show impaired IL-27 signaling in a large cohort of T1D patients (n = 51) compared to age- and gender-matched healthy donors. Increased expression of the IL-27 receptor subunit IL-27Ralpha mRNA in purified myeloid DCs (mDCs), detected by gene expression microarrays was mirrored by enhanced signal transduction in T1D mDCs in response to IL-27 stimulation. Higher STAT phosphorylation in T1D patients was also accompanied by elevated expression of the inhibitory molecules PD-L1, PD-L2 and PD-1, which may suggest not only immunomodulatory mechanisms of IL-27 in T1D but also a compensatory effort of T1D dendritic cells against the ongoing inflammation.
Citace poskytuje Crossref.org
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