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 Blood, 1 December 2008, Vol. 112, No. 12, pp. 4420-4424.
Prepublished online as a Blood First Edition Paper on August 5, 2008; DOI 10.1182/blood-2007-12-126888.

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CHEMOKINES, CYTOKINES, AND INTERLEUKINS

Brief Report

Dendritic cell and natural killer cell cross-talk: a pivotal role of CX3CL1 in NK cytoskeleton organization and activation

Jean R. Pallandre1, Konrad Krzewski2, Romain Bedel1, Bernhard Ryffel3, Anne Caignard4, Pierre Simon Rohrlich1, Xavier Pivot1,5, Pierre Tiberghien1, Laurence Zitvogel6, Jack L. Strominger2, and Christophe Borg1,5

1 Inserm U645, EFS Bourgogne Franche Comté, University of Franche-Comté, IFR133, Besançon, France; 2 Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA; 3 GEM2358, CNRS, Orleans, France; 4 Inserm U753, Institut Gustave Roussy, Villejuif, France; 5 Department of Medical Oncology, CHU Jean Minjoz, Besançon, France; and 6 Inserm U805, Institut Gustave Roussy, Villejuif, France

Initial molecular events leading to natural killer lymphocyte (NK) and dendritic cell (DC) interactions are largely unknown. Here, the role of CX3CL1 (fractalkine), a chemokine expressed on mature dendritic cells (mDCs) has been investigated. We show that CX3CL1 promotes NK activation by mDCs. After blocking of CX3CL1 by antibody, no activation occurred but major histocompatibility complex (MHC) class I neutralization restored DC-mediated NK activation, suggesting an interaction between CX3CL1 signaling and the functioning of inhibitory KIR. Then the YTS NK cell line, in which the inhibitory receptor KIR2DL1 had been introduced, was used. The presence of KIR2DL1 did not decrease YTS activation by HLA-Cw4 DC when CX3CL1 was functional. In contrast, CX3CL1 neutralization led to killer cell immunoglobulin-like receptor (KIR) phosphorylation and SHP-1 recruitment in YTSKIR2DL1 cultured with HLA-Cw4 mDCs. Moreover, CX3CL1 neutralization promoted dispersion of lipid rafts and the formation of a multiprotein complex required for cytoskeletal rearrangements in YTS NK cells. These findings point to a pivotal role of CX3CL1 in the activation of resting NK cells by mature DCs.


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