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and VCAM-1 and Is Rapidly Down-Regulated by a Mechanism Involving T Cells and Expression of Fas1 ,2
*
Laboratory of Experimental Immunology, Division of Basic Sciences, and
Science Applications International Corp. Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702;
Pediatric Oncology Branch, National Institutes of Health, Bethesda, MD 20892; and
§
Department of Oncology, Hoffmann-La Roche, Inc., Nutley, NJ 07110
NK cells have been shown to be important antitumor or antiviral
effector cells in the liver. In the present study we have examined the
factors that regulate the initial recruitment and subsequent fate of
hepatic NK and T cells in mice treated with IL-12 or IL-2. Daily
administration of IL-12 caused a rapid initial increase in NK cells
followed by a subsequent decrease that coincided with an accumulation
of T cells. The recruitment of hepatic NK cells by IL-12, but not the
subsequent T cell infiltrate, was abrogated in IFN-
-/-
mice. In contrast, daily administration of IL-2 caused a sustained
increase in liver-associated NK cells that was not diminished in
IFN--/- mice. The IL-12-induced recruitment in both
hepatic NK and T cells was abrogated by in vivo treatment with
anti-VCAM-1 mAbs, while treatment with anti-ICAM-1 Abs
decreased only the recruitment of T cells in the IL-12-treated mice.
The rapid loss of newly recruited hepatic NK cells in IL-12-treated
mice did not occur in SCID mice or in
B.MRL-Faslpr
(Fas-) and
B6Smn.C3H-Faslgld
(FasL-) mutant mice, suggesting that T cells can actively
eliminate hepatic NK cells through a Fas-dependent mechanism. These
findings also imply that during the endogenous innate immune response
to infectious agents or tumors or in the host response induced by
cytokine therapies, the biologic effects of NK cells may be limited by
T cell-mediated effects.
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