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Role for Tyrosine Phosphorylation and Lyn Tyrosine Kinase in Fas
Receptor-Mediated Apoptosis in Eosinophils
Hans-Uwe Simon,
Shida Yousefi,
Birgit Dibbert,
Holger Hebestreit,
Martina Weber,
Donald R. Branch,
Kurt Blaser,
Francesca Levi-Schaffer, and
Gary P. Anderson
From the Swiss Institute of Allergy and Asthma Research (SIAF),
University of Zurich, Davos, Switzerland; the Research Section,
Canadian Red Cross Society, Toronto, Ontario, Canada; the Department of
Pharmacology, School of Pharmacy, Hebrew University-Hadassah Medical
School, Jerusalem, Israel; and the Department of Pharmacology,
University of Melbourne, Parkville, Victoria, Australia.
Fas ligand/Fas receptor molecular interactions have been implicated
as having an important function for the regulation of eosinophil
apoptosis. The purpose of the present study was to investigate
biochemical events triggered by the engagement of the Fas receptor in
freshly isolated human and mouse eosinophils. Activation of the Fas
receptor on eosinophils with the agonistic anti-Fas monoclonal antibody
(MoAb) resulted in increased tyrosine phosphorylation of several
intracellular proteins. The tyrosine kinase inhibitors lavendustin A
and genistein inhibited Fas receptor-induced cell death in both human
and mouse eosinophils in vitro and prevented, at least partially, Fas
receptor-mediated resolution of eosinophilic inflammation in a mouse in
vivo model of lung eosinophilia. In addition, in freshly purified human
eosinophils, lavendustin A prevented anti-Fas MoAb-induced proteolytic
cleavage of lamin B, suggesting that tyrosine kinases may amplify the
proteolytic signaling cascade within interleukin-1 converting enzyme
(ICE) family proteases. Moreover, the tyrosine kinase Lyn was
identified as being involved in Fas receptor-mediated cell death.
Collectively, these results demonstrate that tyrosine phosphorylation
is an important step in the generation of the Fas receptor-linked
transmembrane death signal in eosinophils and that Lyn participates in
this pathway.
Blood, Vol. 92 No. 2 (July 15), 1998:
pp. 547-557
© 1998 by the American Society of Hematology.
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