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-Facilitated Rejection of Murine B16 Melanomas1
Institutes of
*
Medical Microbiology and
Pathology, University of Ulm, Ulm, Germany
The murine melanoma cell line B16.F10 (H-2b) was
used to study specific T cell responses that reject tumors. Stable B16
transfectants were established that express viral Ags, either the
hepatitis B surface Ag (HBsAg) or the large tumor Ag (T-Ag) of SV40.
B16 cells and their transfected sublines were
CD40+CD44+ but expressed no (or low levels of
the) costimulator molecules CD154 (CD40L), CD48, CD54, CD80, and CD86.
Surface expression of MHC class I (Kb, Db) and
class II (I-Ab) molecules by B16 cells was low, but
strikingly up-regulated by IFN-
. CD95 (Fas) and CD95 ligand (CD95L
(FasL)) were "spontaneously" expressed by B16 cells growing in
vitro in serum-free medium; these markers were strikingly up-regulated
by IFN-. B16 cells coexpressing CD95 and CD95L were irreversibly
programed for apoptosis. In vitro, noninduced B16 transfectants
stimulated a specific IFN- release response, but no cytolytic
response (in a 4-h assay) in MHC class I-restricted CTL; in contrast,
IFN--induced B16 targets were efficiently and specifically lysed by
CTL. In vivo, B16 transfectants were specifically rejected by
DNA-vaccinated syngeneic hosts through a T-dependent immune effector
mechanism. The tumors showed evidence of massive apoptosis in vivo
during the rejection process. The data suggest that CTL-derived IFN-
enhances an intrinsic suicide mechanism of these tumor cells in
addition to facilitating lytic interactions of effectors with tumor
targets.
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