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*
Hospital for Special Surgery, Cornell University Medical Center, New York, NY 10021; and
The Rockefeller University, New York, NY 10021
Immunoregulation of lymphocytes and macrophages in the peripheral
immune system is achieved in part by activation-induced cell death.
Members of the TNF receptor family including Fas (CD95) are involved in
the regulation of activation-induced cell death. To determine whether
activation-induced cell death plays a role in regulation of dendritic
cells (DCs), we examined interactions between Ag-presenting murine DCs
and Ag-specific Th1 CD4+ T cells. Whereas mature bone
marrow- or spleen-derived DCs expressed high levels of Fas, these DCs
were relatively insensitive to Fas-mediated killing by the agonist mAb,
Jo-2, as well as authentic Fas ligand expressed on the CD4+
T cell line, A.E7. The insensitivity to Fas-mediated apoptosis was not
affected by priming with IFN-
and/or TNF-
or by blocking the DC
survival signals TNF-related activation-induced cytokine and CD40L.
However, apoptosis could be induced with C2-ceramide, suggesting that
signals proximal to the generation of ceramide might mediate resistance
to Fas. Analysis of protein expression of several anti-apoptotic
mediators revealed that expression of the intracellular inhibitor of
apoptosis Fas-associated death domain-like IL-1-converting
enzyme-inhibitory protein was significantly higher in Fas-resistant DCs
than in Fas-sensitive macrophages, suggesting a possible role for
Fas-associated death domain-like IL-1-converting enzyme-inhibitory
protein in DC resistance to Fas-mediated apoptosis. Our results
demonstrate that murine DCs differ significantly from other APC
populations in susceptibility to Fas-mediated apoptosis during cognate
presentation of Ag. Because DCs are most notable for initiation of an
immune response, resistance to apoptosis may contribute to this
function.
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