Ibrutinib Blocks CD40 Signaling in CLL In Vivo by Reducing TRAF4 Levels
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F65269705%3A_____%2F21%3A00075061" target="_blank" >RIV/65269705:_____/21:00075061 - isvavai.cz</a>
Výsledek na webu
<a href="https://www.tandfonline.com/doi/abs/10.1080/10428194.2021.1995175" target="_blank" >https://www.tandfonline.com/doi/abs/10.1080/10428194.2021.1995175</a>
DOI - Digital Object Identifier
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Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Ibrutinib Blocks CD40 Signaling in CLL In Vivo by Reducing TRAF4 Levels
Popis výsledku v původním jazyce
Introduction: It has been shown that ibrutinib in vivo limits the proliferative capacity of CLL cells. Here we tested if this effect is due to ibrutinib's effect on CLL-T cell interaction, especially CD40 signaling, which is well-known to induce B cell proliferation in vitro and in vivo. It has been previously noted that CLL cells exposed to ibrutinib in vitro have a decreased CD40 responsiveness (Slinger et al., 2017). Conclusion: We describe that therapy with the BCR inhibitor ibrutinib impairs the responsiveness of CLL cells to the CD40 ligand produced by T cells. We provide mechanistic evidence that this is due to the repression of a novel CD40 pathway regulator, namely TRAF4, via induction of miR-29.
Název v anglickém jazyce
Ibrutinib Blocks CD40 Signaling in CLL In Vivo by Reducing TRAF4 Levels
Popis výsledku anglicky
Introduction: It has been shown that ibrutinib in vivo limits the proliferative capacity of CLL cells. Here we tested if this effect is due to ibrutinib's effect on CLL-T cell interaction, especially CD40 signaling, which is well-known to induce B cell proliferation in vitro and in vivo. It has been previously noted that CLL cells exposed to ibrutinib in vitro have a decreased CD40 responsiveness (Slinger et al., 2017). Conclusion: We describe that therapy with the BCR inhibitor ibrutinib impairs the responsiveness of CLL cells to the CD40 ligand produced by T cells. We provide mechanistic evidence that this is due to the repression of a novel CD40 pathway regulator, namely TRAF4, via induction of miR-29.
Klasifikace
Druh
O - Ostatní výsledky
CEP obor
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OECD FORD obor
30204 - Oncology
Návaznosti výsledku
Projekt
<a href="/cs/project/NU20-03-00292" target="_blank" >NU20-03-00292: PRIORITIZACE KOMBINACÍ LÉČIV U CHRONICKÉ LYMFOCYTÁRNÍ LEUKÉMIE NA ZÁKLADĚ ANALÝZY ADAPTACE BUNĚK NA IBRUTINIB A IDELALISIB IN VIVO</a><br>
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2021
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů