T-cell activation triggers death receptor-6 expression in a NF-kappa B and NF-AT dependent manner

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F11%3A00371708" target="_blank" >RIV/68378050:_____/11:00371708 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.molimm.2011.03.021" target="_blank" >http://dx.doi.org/10.1016/j.molimm.2011.03.021</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.molimm.2011.03.021" target="_blank" >10.1016/j.molimm.2011.03.021</a>

Jazyk výsledku

angličtina

Název v původním jazyce

T-cell activation triggers death receptor-6 expression in a NF-kappa B and NF-AT dependent manner

Popis výsledku v původním jazyce

Death receptor-6 (DR6) participates in the regulation of T-cell activation and/or activity as its genetic disruption results in enhanced CD4+ T-cell expansion, the production of Th2 cytokines, and interestingly also the compromised migration of CD4+ T cells to sites of inflammation. In this communication we show that DR6 is not expressed in resting T cells from human peripheral blood or murine lymph nodes but that its expression is significantly upregulated in CD3 crosslinking- or PMA/ionomycin-activated T lymphocytes. DR6 expression is transiently increased in both activated human CD4+ and CD8+ T cells and it is apparently dependent on the activation of NF-kappaB and NF-AT signaling pathways. In contrast to primary peripheral blood T cells, the widelyused model lymphoblastic leukemia T-cell line Jurkat is DR6-positive and unexpectedly, TCR-mediated stimulation of Jurkat cells strongly downregulates DR6 expression via suppression of its transcription.

Název v anglickém jazyce

T-cell activation triggers death receptor-6 expression in a NF-kappa B and NF-AT dependent manner

Popis výsledku anglicky

Death receptor-6 (DR6) participates in the regulation of T-cell activation and/or activity as its genetic disruption results in enhanced CD4+ T-cell expansion, the production of Th2 cytokines, and interestingly also the compromised migration of CD4+ T cells to sites of inflammation. In this communication we show that DR6 is not expressed in resting T cells from human peripheral blood or murine lymph nodes but that its expression is significantly upregulated in CD3 crosslinking- or PMA/ionomycin-activated T lymphocytes. DR6 expression is transiently increased in both activated human CD4+ and CD8+ T cells and it is apparently dependent on the activation of NF-kappaB and NF-AT signaling pathways. In contrast to primary peripheral blood T cells, the widelyused model lymphoblastic leukemia T-cell line Jurkat is DR6-positive and unexpectedly, TCR-mediated stimulation of Jurkat cells strongly downregulates DR6 expression via suppression of its transcription.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

<a href="/cs/project/1M0506" target="_blank" >1M0506: Centrum molekulární a buněčné imunologie</a><br>

Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2011

Kód důvěrnosti údajů

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

Název periodika

Molecular Immunology

ISSN

0161-5890

e-ISSN

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Svazek periodika

48

Číslo periodika v rámci svazku

12

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

9

Strana od-do

1439-1447

Kód UT WoS článku

000292444100011

EID výsledku v databázi Scopus

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