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Thomas E. Starzl Transplantation Institute and Department of Surgery, and
Department of Molecular Genetics and Biochemistry, University of Pittsburgh, Pittsburgh, PA 15213
There is evidence that donor-derived dendritic cells (DC),
particularly those at a precursor/immature stage, may play a role in
the immune privilege of liver allografts. Underlying mechanisms are
poorly understood. We have examined the influence of in vitro generated
mouse liver-derived DC progenitors (DCp) on proliferative, cytotoxic,
and Th1/Th2 cytokine responses induced in allogeneic T cells. Liver
DCp, propagated in GM-CSF from C57B10 mice (H2b), induced
only minimal proliferation, and weak cytotoxic responses in allogeneic
(C3H; H2k) T cells compared with mature bone marrow
(BM)-derived DC. Flow-cytometric analysis of intracellular cytokine
staining revealed that mature BM DC, but not liver DCp, elicited
CD4+ T cell production of IFN-
. Intracellular expression
of IL-10 was very low in both BM DC- and liver DCp-stimulated
CD4+ T cells. Only stimulation by liver DCp was associated
with IL-10 secretion in primary MLR. Notably, these liver DCp
cocultured with allogeneic T cells stained strongly for IL-10.
Following local (s.c.) injection in allogeneic recipients, both BM DC
and liver DCp homed to T cell areas of draining lymph nodes and spleen,
where they were readily detected by immunohistochemistry up to 2 wk
postinjection. Liver DCp induced clusters of IL-10- and IL-4-secreting
mononuclear cells, whereas Th2 cytokine-secreting cells were not
detected in mice injected with mature BM DC. By contrast, comparatively
high numbers of IFN-+ cells were induced by BM DC.
Modulation of Th2 cytokine production by donor-derived DCp may
contribute to the comparative immune privilege of hepatic
allografts.
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