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*
Institut National de la Santé et de la Recherche Médicale, Unit 429, Hôpital Necker-Enfants Malades, Paris, France;
National Institute for Medical Research, The Ridgeway, Mill Hill, London, United Kingdom; and
Institute Pasteur, Paris, France
2 Current address: Babraham Institute, Babraham, Cambridge, U.K.
Syk and ZAP-70 subserve nonredundant functions in B and T
lymphopoiesis. In the absence of Syk, B cell development is blocked,
while T cell development is arrested in the absence of ZAP-70. The
receptors and the signaling molecules required for differentiation of
NK cells are poorly characterized. Here we investigate the role of the
Syk protein tyrosine kinase in NK cell differentiation. Hemopoietic
chimeras were generated by reconstituting alymphoid (B-,
T-, NK-) recombinase-activating gene-2
x common cytokine receptor 
-chain double-mutant mice with
Syk-/- fetal liver cells. The
phenotypically mature Syk-/- NK cells that
developed in this context were fully competent in natural cytotoxicity
and in calibrating functional inhibitory receptors for MHC molecules.
Syk-deficient NK cells demonstrated reduced levels of Ab-dependent
cellular cytotoxicity. Nevertheless,
Syk-/- NK cells could signal
through NK1.1 and 2B4 activating receptors and expressed ZAP-70
protein. We conclude that the Syk protein tyrosine kinase is not
essential for murine NK cell development, and that compensatory
signaling pathways (including those mediated through ZAP-70) may
sustain most NK cell functions in the absence of
Syk.
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