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Christian Münz^*, Nicholas Holmes, Ashley King, Yung Wai Loke, Marco Colonna^||, Hansjörg Schild^*, and Hans-Georg Rammensee^*

From the ^* Department of Immunology, Institute for Cell Biology, University of Tübingen, 72076 Tübingen, Federal Republic of Germany; Division of Immunology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom; Research Group in Human Reproductive Immunobiology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom; and the ^|| Basel Institute for Immunology, CH-4005 Basel, Switzerland

The crucial immunological function of the classical human major histocompatibility complex (MHC) class I molecules, human histocompatibility leukocyte antigen (HLA)-A, -B, and -C, is the presentation of peptides to T cells. A secondary function is the inhibition of natural killer (NK) cells, mediated by binding of class I molecules to NK receptors. In contrast, the function of the nonclassical human MHC class I molecules, HLA-E, -F, and -G, is still a mystery. The specific expression of HLA-G in placental trophoblast suggests an important role for this molecule in the immunological interaction between mother and child. The fetus, semiallograft by its genotype, escapes maternal allorecognition by downregulation of HLA-A and HLA-B molecules at this interface. It has been suggested that the maternal NK recognition of this downregulation is balanced by the expression of HLA-G, thus preventing damage to the placenta. Here, we describe the partial inhibition of NK lysis of the MHC class I negative cell line LCL721.221 upon HLA-G transfection. We present three NK lines that are inhibited via the interaction of their NKAT3 receptor with HLA-G and with HLA-Bw4 molecules. Inhibition can be blocked by the anti-NKAT3 antibody 5.133. In conclusion, NK inhibition by HLA-G via NKAT3 may contribute to the survival of the fetal semiallograft in the mother during pregnancy.

This work was supported by grants from the Deutsche Forschungsgemeinschaft (Leibnizprogramm, Ra 369/ 4-1) and from the Bundesministerium für Bildung, Wissenschaft und Technologie.

¹Abbreviations used in this paper: KAR, killer activatory receptor; KIR, killer inhibitory receptor; LGL, large granular lymphocyte.

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