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Production Are Not Always Coordinately Regulated: Engagement of DX9 KIR+ NK Cells by HLA-B7 Variants and Target Cells1
Departments of
*
Pathology,
Oral Pathology, Radiology, and Medicine, and
Microbiology and the
§
Immunology and Molecular Biology Graduate Programs, University of Iowa, Iowa City, IA 52242, and
¶
The Basel Institute for Immunology, Basel, Switzerland
DX9 mAb-binding killer cell-inhibitory receptors (KIR) recognize
HLA-B molecules that express the Bw4 public serologic epitope. We
assessed DX9+ NK cell fine specificity recognition of
HLA-B7 variants and HLA-B27 alleles by 51Cr release natural
cytotoxicity assays and by flow cytometry and enzyme-linked immunospot
(ELISPOT) IFN-
synthesis and release assays. 721.221 target cell
expression of Bw4+ HLA-B27 alleles specifically inhibited
DX9+ NK cell natural cytotoxicity and IFN- synthesis and
release. A triple substitution of HLA-B7 at residues 80, 82, and 83
known to induce expression of the Bw4 serologic epitope also
specifically inhibited DX9+ NK cell natural cytotoxicity
and IFN- responses. Single HLA-B7 amino acid substitution variants
were recognized in the same decreasing rank order by DX9+
NK cells and Bw4-reactive mAbs: G83R > R82L > N80T =
HLA-B7. Natural cytotoxicity inhibition was reversed by the presence of
blocking DX9 mAb. Natural cytotoxicity and IFN- production were
coordinately regulated by a panel of HLA-B7 variants expressed on
721.221 cells, suggesting that these two effector functions are
inhibited by the same KIR-mediated signaling mechanisms. In contrast,
some NK cell clones killed 721.221 and K562 target cells equally well
but released much more IFN- in response to K562 target cells.
Differential regulation of natural cytotoxicity and IFN- release
shows that NK cell effector functions respond to distinct signals.
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