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T Cells, and Antigen-Specific CTL1
*
Department of Immunobiology, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304; and
Department of Tumor Immunology, University Hospital Nijmegen, Nijmegen, The Netherlands
NK cells and T cells express killer cell inhibitory receptors (KIR)
recognizing polymorphic MHC class I molecules. Although prior studies
have established that MHC class I can protect normal and transformed
hematopoietic cells from NK cell lysis, the role of MHC class I on the
recognition of solid tumors has been controversial. In this study, we
investigated whether interactions of KIR with their ligands on melanoma
tumor cells could inhibit tumor cell lysis by NK and 
T cell
clones. Ligation of the NK cell receptor KIR3DL1 by HLA-Bw4 allotypes
resulted in inhibition of cytotoxicity against HLA-B*4403-transfected
melanomas as well as against melanomas endogenously expressing HLA-Bw4
allotypes. Similarly, interactions of KIR2DL2 or KIR2DL3 (KIR2DL2/3)
with HLA-Cw3-related allotypes on melanomas resulted in decreased tumor
cell lysis. We also investigated whether signaling via KIR affected
melanoma recognition by CTL. Introduction of KIR3DL1 molecules into
HLA-A*0201-restricted gp100-specific CTL resulted in inhibition of
lysis of gp100+ melanomas co-expressing HLA-A*0201
and HLA-Bw4 allotypes. These results suggest that disrupting
interactions of KIR with their ligands on tumor cells in vivo may
enhance antitumor responses mediated by both innate and adaptive immune
effector cells.
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