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Qa-1^b-Dependent Modulation of Dendritic Cell and NK Cell Cross-Talk In Vivo¹

Paula Colmenero^2,*, Angela L. Zhang^*, Ting Qian^*, Linrong Lu, Harvey Cantor, Kalle Söderström^* and Edgar G. Engleman^*

^* Department of Pathology, Stanford University School of Medicine, Palo Alto, CA 94304; and Department of Cancer Immunology and AIDS, Dana–Farber Cancer Institute, Harvard Medical School, Boston, MA 02115

Dendritic cells (DC) trigger activation and IFN- release by NK cells in lymphoid tissues, a process important for the polarization of Th1 responses. Little is known about the molecular signals that regulate DC-induced NK cell IFN- synthesis. In this study, we analyzed whether the interaction between Qa-1^b expressed on DC and its CD94/NKG2A receptor on NK cells affects this process. Activation of DC using CpG-oligodeoxynucleotides in Qa-1^b-deficient mice, or transfer of CpG-oligodeoxynucleotide-activated Qa-1^b-deficient DC into wild-type mice, resulted in dramatically increased IFN- production by NK cells, as compared with that induced by Qa-1^b-expressing DC. Masking the CD94/NKG2A inhibitory receptor on NK cells in wild-type mice similarly enhanced the IFN- response of these cells to Qa-1^b-expressing DC. Furthermore, NK cells from CD94/NKG2A-deficient mice displayed higher IFN- production upon DC stimulation. These results demonstrate that Qa-1^b is critically involved in regulating IFN- synthesis by NK cells in vivo through its interaction with CD94/NKG2A inhibitory receptors. This receptor-ligand interaction may be essential to prevent unabated cytokine production by NK cells during an inflammatory response.

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 National Institutes of Health Grants HL57443, AR051748, and AI055468.

² Address correspondence and reprint requests to Dr. Paula Colmenero, Department of Pathology, Stanford Blood Center, Stanford University, 3373 Hillview Avenue, Palo Alto, CA 94304-1204. E-mail address: paucol{at}stanford.edu

³ Abbreviations used in this paper used in this paper: DC, dendritic cell; ODN, oligodeoxynucleotide; LN, lymph node; BM-DC, bone marrow-derived DC; WT, wild type.

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