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Data on microbial DNA-induced IL-1β production in monocytes of type 1 diabetes patients
I. Zentsova, Z. Parackova, J. Kayserova, L. Palova-Jelinkova, P. Vrabcova, N. Volfova, Z. Sumnik, S. Pruhova, L. Petruzelkova, A. Sediva,
Jazyk angličtina Země Nizozemsko
Typ dokumentu časopisecké články
Grantová podpora
NV16-32838A
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Free Medical Journals od 2014-12-01
PubMed Central od 2014
Europe PubMed Central od 2014 do 2020
Open Access Digital Library od 2014-12-01
Open Access Digital Library od 2014-01-01
Open Access Digital Library od 2014-01-01
Elsevier Open Access Journals od 2014-12-01
ROAD: Directory of Open Access Scholarly Resources od 2014
Odkazy
PubMed
31453296
DOI
10.1016/j.dib.2019.104321
Knihovny.cz E-zdroje
- Publikační typ
- časopisecké články MeSH
Inflammasomes are large protein complexes involved in the maturation of IL-1β, a cytokine associated with the pathophysiology of type 1 diabetes (T1D). The data presented in this article focused on the role of inflammasomes in DNA recognition in T1D patients. This data extend knowledge on DNA sensing in T1D patients and relate to our research paper "Monocytes contribute to DNA sensing through the TBK1 signaling pathway in type 1 diabetes patients" Zentsova et al., 2009. To examine inflammasome involvement, we blocked the known mechanism of inflammasome activation - potassium efflux via various approaches: 1) high concentration of KCl; 2) Glybenclamide, which selectively blocks the ATP sensitive K+ channel; 3) KN-62, an inhibitor of P2X7 receptor, which activates K+ channel after ATP binding. Moreover, we used an inhibitor which blocks Nod-like receptor family containing pyrin domain 3 (NLRP3) inflammasome. In T1D patients, we show that secretion of cytokines IL-1β, TNFα, IL-6 and IFNα after microbial DNA stimulation is promoted by potassium efflux and is not dependent on P2X7 receptor signaling. Surprisingly, the microbial DNA induced IL-1β release was independent of NLRP3.
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