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(Mig) and Chemokine Responsive to -2 (Crg-2)1
*
Laboratory of Experimental Immunology, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702;
IRSP, Science Applications International Corporation, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702;
Pediatric Oncology Branch, National Institutes of Health, Bethesda, MD;
Greenbaum Cancer Center, University of Maryland Medical School, Baltimore, MD; and
¶ Laboratory of Molecular Immunoregulation, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702
The IFN-
-inducible proteins monokine induced by IFN- (Mig)
and chemokine responsive to -2 (Crg-2) can contribute to
IL-12-induced antiangiogenic and leukocyte-recruiting activities, but
the extent to which leukocytes vs parenchymal cells in different organs
contribute to the production of these molecules remains unclear. The
results presented herein show that IFN--dependent induction of Mig
and Crg-2 gene expression can occur in many nonlymphoid organs, and
these genes are rapidly induced in purified hepatocytes isolated from
mice treated with IL-2 plus IL-12, or from Hepa 1-6 hepatoma cells
treated in vitro with IFN-. In addition to depending on IFN-, the
ability of IL-12 or IL-2/IL-12 to induce Mig and Crg-2 gene expression
in purified hepatocytes also is accompanied by the coordinate
up-regulation of the IFN- R 
and 
-chains, in the absence of
IL-12R components. Supernatants of primary hepatocytes obtained from
mice treated in vivo with IL-2/IL-12 or from hepatocytes treated in
vitro with IFN- contain increased chemotactic activity for enriched
human and mouse CD3+ T cells, as well as mouse
DX5+ NK cells. The hepatocyte-derived chemotactic activity
for mouse T cells but not NK cells was ablated by Abs specific for Mig
and Crg-2. These results suggest that parenchymal cells in some organs
may contribute substantially to initiation and/or amplification of
inflammatory or antitumor responses.
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