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Departments of
*
Medicine and
Cell Biology, Washington University School of Medicine, St. Louis, MO 63110
Over activation of CD4+ T cells in the peripheral blood
and airway tissues is characteristic of asthma; therefore, we
investigated whether activated T cells from asthmatic subjects have
altered apoptotic potential through the Fas death receptor. We found
that mitogen-stimulated peripheral blood T cells of asthmatic subjects
expressed cell surface Fas, but failed to undergo the normal degree of
apoptosis after Fas receptor ligation. T cells from asthmatics
exhibited normal apoptotic responses to 
-irradiation (dependent on
IL-1 converting enzyme family proteases), ceramide, and mitogen
challenge, suggesting functional integrity of the apoptotic pathway.
Furthermore, the defect in Fas-dependent apoptosis was overcome by
prestimulation with allogeneic accessory cells instead of mitogen.
Taken together, the findings suggest that selective resistance to
Fas-dependent apoptosis reflects altered Ag-driven, accessory
cell-dependent signaling and that ineffective activation of Fas signal
transduction may contribute to T cell-dependent immunoinflammation in
asthma.
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