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Cutting Edge: Killer Ig-Like Receptors Mediate "Missing Self" Recognition In Vivo¹

Jeroen van Bergen^2,*, Allan Thompson^*, Christelle Retière, John Trowsdale and Frits Koning^*

^* Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands; Immunology Division, Department of Pathology, Cambridge University, Cambridge, United Kingdom; and Etablissement Français du Sang, Immunovirologie et polymorphisme génétique, EA4271, Nantes, France

Although it is well established that human NK cells are able to detect the absence of autologous HLA class I in vitro by virtue of inhibitory killer Ig-like receptors (KIR), direct evidence that KIR can mediate "missing self" recognition in vivo is lacking. To test this, we generated mice transgenic for a human KIR B-haplotype and HLA-Cw3 on a C57BL/6 background. NK cells in these mice expressed multiple KIR in a stochastic manner, including the HLA-Cw3-specific inhibitory receptor KIR2DL2. KIR and HLA transgenic mice rejected wild-type C57BL/6 spleen cells upon i.v. injection. This rejection was dependent on the presence of the KIR transgene in the host and on the absence of HLA-Cw3 from the injected target cells. Hence, the KIR transgene mediated "missing self" recognition in vivo. We anticipate that this KIR and HLA transgenic mouse will help shed light on KIR and HLA effects in disease and transplantation.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Landsteiner Grant 0515 (to J.v.B.).

² Address correspondence and reprint requests to Jeroen van Bergen, Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands. E-mail address: J.van_Bergen{at}lumc.nl

³ Abbreviation used in this paper: KIR, killer Ig-like receptor.