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Editorials
References
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Granulocyte colony-stimulating factor acts on lymphoid-biased, short-term hematopoietic stem cells
Yulin Chen and K. Lenhard Rudolph
Leibniz Institute on Aging - Fritz Lipmann Institute (FLI), Research Group on Stem Cell Aging, Jena and Medical Faculty, University Hospital Jena (UKJ), Jena, Germany
E-mail: K. LENHARD RUDOLPH - lenhard.rudolph@leibniz-fli.de doi:10.3324/haematol.2020.271205
Granulocyte colony-stimulating factor (G-CSF) is a cytokine that increases myelopoiesis,1 impairs lym- phopoiesis by inhibiting committed progenitor cells,2,3 and enhances hematopoietic stem cell (HSC) mobi- lization.4 The direct effects of G-CSF on purified subpopu- lation of HSC remained to be delineated. In this issue of Haematologica, Xie et al.5 investigate the influence of G-CSF on proliferation and the repopulating potential of myeloid- biased, long-term HSC (CD201+CD150+CD48–CD41– CD34–KSL) and lymphoid-biased, short-term HSC (CD201+CD150–CD48–CD41–CD34–KSL).
Understanding the direct influences of G-CSF on HSC could improve our understanding of HSC responses to an increase in G-CSF level caused by inflammation.6 The study by Xie et al. shows that G-CSF acts directly on lym- phoid-biased, short-term HSC but not on myeloid-biased HSC. Interestingly, G-CSF cooperates with stem cell fac- tor in driving the expansion of lymphoid-biased, short- term HSC in culture and in maintaining the in vivo repop- ulating potential of such cultures. These findings suggest that G-CSF-mediated effects on lymphoid-biased, short- term HSC may contribute to the previously noted
enhancement of early lymphopoiesis of bone marrow stem and progenitor cells after exposure to G-CSF.7 In contrast, however, G-CSF is also known to instruct bone marrow stromal cells to suppress the function of commit- ted progenitors of B-lymphopoiesis.2 The functional rele- vance of the G-CSF-mediated priming of early lymphoid progenitor cells and lymphoid-biased HSC5,7 in associa- tion with G-CSF-mediated impairment in the progression of lymphopoiesis from committed progenitor cells2 should be delineated in future studies.
The primary role of G-CSF is currently seen in activa- tion of myelopoiesis to strengthen myeloid immune responses, such as the recruitment of neutrophils during bacterial lung infections.8 However, the simultaneous priming of early lymphoid progenitor cells and lymphoid- biased HSC by G-CSF may also be important to ensure prompt reactivation of lymphopoiesis after the initial induction of myeloid cell-driven immune responses. The sequential coordination of such immune actions by G- CSF seems to be an interesting area of future research.
Understanding direct influences of G-CSF on HSC could also be relevant for our understanding of HSC
haematologica | 2021; 106(6)