Data on microbial DNA-induced IL-1β production in monocytes of type 1 diabetes patients

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064165%3A_____%2F19%3A10398494" target="_blank" >RIV/00064165:_____/19:10398494 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11110/19:10398494 RIV/00216208:11130/19:10398494 RIV/00064203:_____/19:10398494

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=QkMH0vpbyT" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=QkMH0vpbyT</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.dib.2019.104321" target="_blank" >10.1016/j.dib.2019.104321</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Data on microbial DNA-induced IL-1β production in monocytes of type 1 diabetes patients

Popis výsledku v původním jazyce

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 &quot;Monocytes contribute to DNA sensing through the TBK1 signaling pathway in type 1 diabetes patients&quot; 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.

Název v anglickém jazyce

Data on microbial DNA-induced IL-1β production in monocytes of type 1 diabetes patients

Popis výsledku anglicky

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 &quot;Monocytes contribute to DNA sensing through the TBK1 signaling pathway in type 1 diabetes patients&quot; 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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30102 - Immunology

Projekt

<a href="/cs/project/NV16-32838A" target="_blank" >NV16-32838A: Buňky vrozené imunity u diabetu mellitu 1. typu: Objasnění role dendritických buněk, monocytů a neutrofilů v patogenezi T1D</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2019

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Data in Brief

ISSN

2352-3409

e-ISSN

—

Svazek periodika

25

Číslo periodika v rámci svazku

August

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

5

Strana od-do

104321

Kód UT WoS článku

000495104500339

EID výsledku v databázi Scopus

2-s2.0-85070221615