Improved hematopoietic stem cell transplantation upon inhibition of natural killer cell-derived interferon-gamma

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F21%3A00555012" target="_blank" >RIV/68378050:_____/21:00555012 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11120/21:43921781 RIV/00216208:11110/21:10429136 RIV/00064165:_____/21:10429136 RIV/00216208:11130/21:10429136 RIV/00216208:11310/21:10429136

Výsledek na webu

<a href="https://linkinghub.elsevier.com/retrieve/pii/S2213671121003143" target="_blank" >https://linkinghub.elsevier.com/retrieve/pii/S2213671121003143</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.stemcr.2021.06.008" target="_blank" >10.1016/j.stemcr.2021.06.008</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Improved hematopoietic stem cell transplantation upon inhibition of natural killer cell-derived interferon-gamma

Popis výsledku v původním jazyce

Hematopoietic stem cell transplantation (HSCT) is a frequent therapeutic approach to restore hematopoiesis in patients with hematologic diseases. Patients receive a hematopoietic stem cell (HSC)-enriched donor cell infusion also containing immune cells, which may have a beneficial effect by eliminating residual neoplastic cells. However, the effect that donor innate immune cells may have on the donor HSCs has not been deeply explored. Here, we evaluate the influence of donor natural killer (NK) cells on HSC fate, concluded that NK cells negatively affect HSC frequency and function, and identified interferon-gamma (IFNg) as a potential mediator. Interestingly, improved HSC fitness was achieved by NK cell depletion from murine and human donor infusions or by blocking IFNg activity. Thus, our data suggest that suppression of inflammatory signals generated by donor innate immune cells can enhance engraftment and hematopoietic reconstitution during HSCT, which is particularly critical when limited HSC numbers are available and the risk of engraftment failure is high.

Název v anglickém jazyce

Improved hematopoietic stem cell transplantation upon inhibition of natural killer cell-derived interferon-gamma

Popis výsledku anglicky

Hematopoietic stem cell transplantation (HSCT) is a frequent therapeutic approach to restore hematopoiesis in patients with hematologic diseases. Patients receive a hematopoietic stem cell (HSC)-enriched donor cell infusion also containing immune cells, which may have a beneficial effect by eliminating residual neoplastic cells. However, the effect that donor innate immune cells may have on the donor HSCs has not been deeply explored. Here, we evaluate the influence of donor natural killer (NK) cells on HSC fate, concluded that NK cells negatively affect HSC frequency and function, and identified interferon-gamma (IFNg) as a potential mediator. Interestingly, improved HSC fitness was achieved by NK cell depletion from murine and human donor infusions or by blocking IFNg activity. Thus, our data suggest that suppression of inflammatory signals generated by donor innate immune cells can enhance engraftment and hematopoietic reconstitution during HSCT, which is particularly critical when limited HSC numbers are available and the risk of engraftment failure is high.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

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OECD FORD obor

10601 - Cell biology

Projekt

<a href="/cs/project/GA18-08577S" target="_blank" >GA18-08577S: Transkripční factor C/EBPg jako nový regulátor vývoje a funkce žírných buněk</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2021

Kód důvěrnosti údajů

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

Název periodika

Stem Cell Reports

ISSN

2213-6711

e-ISSN

2213-6711

Svazek periodika

16

Číslo periodika v rámci svazku

8

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

15

Strana od-do

1999-2013

Kód UT WoS článku

000684300500013

EID výsledku v databázi Scopus

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