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Dendritic cells (DC) trigger activation and IFN-gamma 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-gamma 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-gamma 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-gamma response of these cells to Qa-1(b)-expressing DC. Furthermore, NK cells from CD94/NKG2A-deficient mice displayed higher IFN-gamma production upon DC stimulation. These results demonstrate that Qa-1(b) is critically involved in regulating IFN-gamma 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.

Original publication

DOI

10.4049/jimmunol.179.7.4608

Type

Journal article

Journal

Journal of immunology (Baltimore, Md. : 1950)

Publication Date

10/2007

Volume

179

Pages

4608 - 4615

Addresses

Department of Pathology, Stanford University School of Medicine, Palo Alto, CA 94304, USA. paucol@stanford.edu

Keywords

Lymph Nodes, Dendritic Cells, Killer Cells, Natural, Cells, Cultured, Animals, Mice, Knockout, Mice, Carrier Proteins, Histocompatibility Antigens Class I, Cell Communication, Cell Movement, Up-Regulation, Interferon-gamma, NK Cell Lectin-Like Receptor Subfamily D