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Blood, 1 October 2000, Vol. 96, No. 7, pp. 2506-2510
IMMUNOBIOLOGY
Syk-deficient eosinophils show normal interleukin-5-mediated
differentiation, maturation, and survival but no longer respond to
Fc R activation
Estelle Lach-Trifilieff,
Keith Menear,
Edina Schweighoffer,
Victor L. J. Tybulewicz, and
Christoph Walker
From the Novartis Horsham Research Centre, Horsham,
England; and National Institute for Medical
Research, London, England.
The tyrosine kinase Syk has been proposed to play a critical role
in the antiapoptotic effect of interleukin (IL)-5 in human eosinophils.
However, little is known about the involvement of Syk in other
IL-5-mediated activation events. To further address these questions,
the role of Syk in IL-5-induced eosinophil differentiation, activation, and survival was analyzed using cells obtained from Syk-deficient mice. We could demonstrate that Syk-deficient fetal liver
cells differentiate into mature eosinophils in response to IL-5 at the
same rate as wild-type fetal liver cells and generate the same total
number of eosinophils. Moreover, no difference in IL-5-induced
survival of mature eosinophils between Syk / and
wild-type eosinophils could be demonstrated, suggesting that the
antiapoptotic effect of IL-5 does not require Syk despite the
activation of this tyrosine kinase upon IL-5 receptor ligation. In
contrast, eosinophils derived from Syk-deficient but not wild-type mice
were incapable of generating reactive oxygen intermediates in response
to Fc receptor (FcR) engagement. Taken together, these data
clearly demonstrate no critical role for Syk in IL-5-mediated eosinophil differentiation or survival but underline the importance of
this tyrosine kinase in activation events induced by FcR stimulation.
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