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Department of Immunology, Robert Koch Institute, Berlin, Germany
Whole spleen cell cultures from SCID mice release high levels of
IFN-
when exposed to heat-killed Listeria
monocytogenes (HKL). This microbe-induced and T
cell-independent response depends on both macrophages (M
) and NK
cells: HKL-stimulated M release TNF-
and IL-12, which together
activate NK cells for IFN- release. We show here that this
cytokine-mediated activation cascade can be modulated by a mAb against
the M surface glycoprotein F4/80. HKL-induced IL-12, TNF-, and
IFN- in SCID whole spleen cell cultures was inhibited by
coincubation with anti-F4/80 mAb whereas IL-1 and IL-10 were
enhanced. Both effects were apparent at mRNA and protein release
levels. Whereas inhibitory activities were F4/80 Ag specific,
stimulatory effects were Fc dependent and nonspecific. Furthermore,
cytokine inhibition by anti-F4/80 was only apparent when M and
NK cells were present simultaneously and in close vicinity, indicating
that direct cell-to-cell contact is a prerequisite. These data suggest
a novel pathway for microbe-induced M/NK cell interaction involving
direct cell-to-cell signaling and give the first evidence for a
functional role of the M surface glycoprotein
F4/80.
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