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Release by Liver NKT Cells1
Departments of
*
Medical Microbiology and Immunology and
Pathology, University of Ulm, Ulm, Germany
A prominent subset of the hepatic innate immune system is
-galactosylceramide (GalCer)-reactive, (CD4+ and
CD4-CD8-) CD1d-restricted NKT cells. We
investigated in C57BL/6 (B6) mice which hepatic cell type stimulates
hepatic NKT cell activation. Surface expression of CD1d but not CD40,
CD80, or CD86 costimulator molecules was detected in hepatocytes.
Pulsed in vitro or in vivo with GalCer, hepatocytes triggered IL-4
release by liver NKT cells but required exogenous IL-12 to trigger
IFN-
release by NKT cells. Liver dendritic cells (DC) isolated from
nontreated mice showed low surface expression of MHC, CD1d, and CD40,
CD80, or CD86 costimulator molecules that were strikingly up-regulated
after GalCer injection. Although liver CD11c+ DC
displayed lower CD1d surface expression than hepatocytes, they were
potent stimulators of IFN- and IL-4 release by liver NKT when pulsed
with GalCer in vitro or in vivo. Liver DC are thus potent
stimulators of proinflammatory cytokine release by NKT cells, are
activated themselves in the process of NKT cell activation, and express
an activated phenotype after the NKT cell population is eliminated
following GalCer stimulation.
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