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*
Department of Medicine, University of Michigan, and
Veterans Affairs Medical Center, Ann Arbor MI 48109
The human marrow produces 
1010 monocytes daily, and
this production must be balanced by a similar rate of destruction.
Monocytes/macrophages can undergo apoptosis after activating
CD4+ T cells, suggesting one mechanism that may contribute
to macrophage homeostasis. Previous reports indicate that Fas-Fas
ligand interactions are the principle molecules mediating this
response. However, D10, an Iak-restricted cloned Th2 line,
will similarly induce apoptosis in Ag-presenting macrophages, and D10
cells lack Fas ligand. To confirm that D10 cells kill macrophages
through Fas-independent pathways, D10 cells were shown to kill MRL
lpr/lpr (Iak) macrophages in an Ag-dependent
fashion, indicating additional mechanisms. Recent reports demonstrate
that TNF-related apoptosis-inducing ligand (TRAIL), interacting with
Apo2, and TNF-like weak inducer of apoptosis (TWEAK), interacting with
Apo3, will induce apoptosis in some cells. Using Abs to TRAIL and an
Apo3-IgG Fc fusion protein, we demonstrated that D10 cells express both
TRAIL and TWEAK. The Apo3 fusion protein, but not human IgG, inhibited
D10-induced macrophage apoptosis, as did anti-TRAIL. Further
studies demonstrated that AE7, a cloned Th1 line, and splenic T cells
express TWEAK, TRAIL, and Fas ligand, and inhibiting these molecules
also inhibited macrophage killing. These results indicate that D10
cells induce macrophage apoptosis through TRAIL- and
TWEAK-dependent pathways. Because normal T cells also express these
molecules, these results support the concept that T cells have multiple
pathways by which to induce macrophage apoptosis. These pathways may be
important in immune processes such as macrophage homeostasis as well as
in down-regulation of immune responses and elimination of
macrophages infected with intracellular
organisms.
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