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*
Thomas E. Starzl Transplantation Institute and Department of Surgery,
Department of Cell Biology and Physiology, and
Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA 15213; and
Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720
Leukocytes resident in the liver may play a role in immune
responses. We describe a cell population propagated from mouse liver
nonparenchymal cells in IL-3 and anti-CD40 mAb that exhibits a
distinct surface immunophenotype and function in directing
differentiation of naive allogeneic T cells. After culture, such cells
are
DEC-205brightB220+CD11c-CD19-,
and negative for T (CD3, CD4, CD8
), NK (NK 1.1) cell markers, and
myeloid Ags (CD11b, CD13, CD14). These liver-derived
DEC205+B220+ CD19- cells have a
morphology and migratory capacity similar to dendritic cells.
Interestingly, they possess Ig gene rearrangements, but lack Ig
molecule expression on the cell surface. They induce low thymidine
uptake of allogeneic T cells in MLR due to extensive apoptosis of
activated T cells. T cell proliferation is restored by addition of the
common caspase inhibitor peptide,
benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk). T cells
stimulated by liver-derived
DEC205+B220+D19- cells release
both IL-10 and IFN-
, small amounts of TGF-
, and no IL-2 or IL-4,
a cytokine profile resembling T regulatory type 1 cells. Expression of
IL-10 and IFN-, but not bioactive IL-12 in liver
DEC205+B220+CD19- cells was
demonstrated by RNase protection assay. In vivo administration of liver
DEC205+B220+CD19- cells
significantly prolonged the survival of vascularized cardiac allografts
in an alloantigen-specific manner.
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