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Clinical and Diagnostic Laboratory Immunology, May 2002, p. 649-657, Vol. 9, No. 3
1071-412X/02/$04.00+0     DOI: 10.1128/CDLI.9.3.649-657.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Activation of Human NK Cells by Staphylococci and Lactobacilli Requires Cell Contact-Dependent Costimulation by Autologous Monocytes

D. Haller,^* P. Serrant, D. Granato, E. J. Schiffrin, and S. Blum

Department of Immunology, Nestlé Research Center, 1000 Lausanne 26, Switzerland

Received 4 October 2001/ Returned for modification 26 November 2001/ Accepted 19 February 2002

NK cells are instrumental in innate immune responses, in particular for the early production of gamma interferon (IFN-) and other cytokines necessary to control certain bacterial, parasitic, and viral infections. NK cell-mediated effector functions are controlled by a fine balance between distinct receptors mediating activating and inhibitory signals; however, little is known about activating receptors on NK cells and their corresponding ligands. Several studies have shown that commensal lactobacilli isolated from the human gastrointestinal tract activate human mononuclear cells and are potent inducers of IFN- and monocyte-derived interleukin 12 (IL-12). NK cell activation was shown for Lactobacillus johnsonii La1. In this study the cellular mechanisms of in vitro NK cell activation by gram-positive bacteria were analyzed. Staphylococcus aureus- and L. johnsonii La1-mediated activation of CD3^- CD16⁺ CD56⁺ human peripheral blood NK cells, including expression of the activation antigen CD69 and secretion of IFN-, required cell contact-dependent costimulation by autologous monocytes. S. aureus- and L. johnsonii-preactivated monocytes retained their capacity to induce NK cell activation. In contrast, cytokine-primed monocytes completely failed to induce NK cell activation unless bacteria were present. This suggests that phagocytosis of bacteria provided additional coactivation signals on accessory cells that may differ from those induced by tumor necrosis factor and IFN-. Blocking of costimulatory molecules by B7.1, B7.2, and IL-12 but not CD14 monoclonal antibodies inhibited S. aureus- and L. johnsonii-induced effector function of NK cells. Our data suggest an important role for accessory cell-derived signals in the process of NK cell activation by gram-positive bacteria.

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* Corresponding author. Mailing address: University of North Carolina, Department of Medicine, 146 Glaxo Building, CB# 7038, Chapel Hill, NC 27599-7038. Phone: (919) 966-7886. Fax: (919) 966-7468. E-mail: hallerdirk{at}hotmail.com.

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Clinical and Diagnostic Laboratory Immunology, May 2002, p. 649-657, Vol. 9, No. 3
1071-412X/02/$04.00+0     DOI: 10.1128/CDLI.9.3.649-657.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

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