The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/11/1841/ $5.00
The Journal of Experimental Medicine, Volume 188, Number 10, November 16, 1998 1841-1848

Articles

Mouse CD94/NKG2A Is a Natural Killer Cell Receptor for the Nonclassical Major Histocompatibility Complex (MHC) Class I Molecule Qa-1b

Russell E. Vance*, Jennifer R. Kraft{ddagger}, John D. Altman§, Peter E. Jensen{ddagger}, and David H. Raulet*

From the * Department of Molecular and Cell Biology and Cancer Research Laboratory, University of California Berkeley, Berkeley, California 94720; and the {ddagger} Department of Pathology and Laboratory Medicine and § Emory Vaccine Center and Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia 30322

Natural killer (NK) cells preferentially lyse targets that express reduced levels of major histocompatibility complex (MHC) class I proteins. To date, the only known mouse NK receptors for MHC class I belong to the Ly49 family of C-type lectin homodimers. Here, we report the cloning of mouse NKG2A, and demonstrate it forms an additional and distinct class I receptor, a CD94/NKG2A heterodimer. Using soluble tetramers of the nonclassical class I molecule Qa-1b, we provide direct evidence that CD94/NKG2A recognizes Qa-1b. We further demonstrate that NK recognition of Qa-1b results in the inhibition of target cell lysis. Inhibition appears to depend on the presence of Qdm, a Qa-1b-binding peptide derived from the signal sequences of some classical class I molecules. Mouse NKG2A maps adjacent to CD94 in the heart of the NK complex on mouse chromosome six, one of a small cluster of NKG2-like genes. Our findings suggest that mouse NK cells, like their human counterparts, use multiple mechanisms to survey class I expression on target cells.

Key Words: CD94 • NKG2A • Qa-1 • natural killer cell • major histocompatibility complex class I

Address correspondence to David H. Raulet, Department of Molecular and Cell Biology, 489 Life Science Addition, University of California, Berkeley, CA 94720. Phone: 510-642-9521; Fax: 510-642-1443; E-mail: raulet{at}uclink4.berkeley.edu

Russell Vance is a Howard Hughes Predoctoral Fellow. This work was supported by National Institutes of Health grants RO1-AI35021 to D.H. Raulet, AI33614 to P.E. Jensen, and RO1-AI42373 to J.D. Altman.

R.E. Vance and J.R. Kraft contributed equally to this work.

Abbreviations used: APC, allophycocyanin; BAC, bacterial artificial chromosomes; HA, hemagglutinin; ITIM, immunoreceptor tyrosine-based inhibitory motif; LAK, IL-2 cultured NK cell; nt, nucleotide; TAP, transporter associated with antigen presentation.


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