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Blood, Vol. 95 No. 3 (February 1), 2000:
pp. 984-991
The receptor tyrosine kinase c-kit provides a critical signal for
survival, expansion, and maturation of mouse natural killer cells
Francesco Colucci and
James P. Di Santo
From the Institut National de la Santè et de la Recherche
Medicale (INSERM) U429, Hôpital Necker-Enfants
Malades, Paris, France.
Fetal liver kinase ligands (flk2L/flt3L) and stem cell factor (SCF)
have been shown to promote natural killer (NK) cell differentiation from hematopoietic stem cell (HSC) precursors in vitro. However, the
contribution of signaling through the receptors for these growth
factors for in vivo NK cell development remains ill-defined. We have
analyzed the role of the SCF receptor c-kit in NK cell differentiation by reconstituting NK-deficient mice with fetal liver
(FL) HSCs of c-kit / (W/W) mice.
Although c-kit/NK cells were generated in
W/W chimeras, they were reduced in number, contained a lower
percentage of CD45R (B220)+ cells, and were poorly
cytolytic. In vitro experiments showed that generation of NK cells from
FL precursors was reduced in the absence of c-kit signaling and that
SCF promoted the survival of peripheral
c-kit+ NK cells. We conclude that c-kit/SCF
interactions in vivo are dispensable for the commitment of HSC to the
NK lineage, but they provide essential signals for generating normal
numbers of fully mature NK cells.
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