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 Blood, 15 September 2005, Vol. 106, No. 6, pp. 2186-2188.
Prepublished online as a Blood First Edition Paper on May 31, 2005; DOI 10.1182/blood-2005-03-1270.

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NEOPLASIA
Brief report

Defective killing of dendritic cells by autologous natural killer cells from acute myeloid leukemia patients

Cyril Fauriat, Alessandro Moretta, Daniel Olive, and Régis T. Costello

From the Laboratoire d'Immunologie des Tumeurs, Institut Paoli-Calmettes, Marseille, France; the Dipartimento di Medicina Sperimentale, Sezione di Istologia, Università degli Studi di Genova, Genova, Italy; the Faculté de Médecine de Marseille, Marseille, France; and the Departement d'Hématologie, Institut Paoli-Calmettes, Marseille, France.

At the frontier between innate and adaptive immunity, dendritic cells (DCs) secrete numerous cytokines and express costimulatory molecules that initiate or enhance natural killer (NK) and T-lymphocyte responses. NK cells also regulate DC physiology by killing immature DCs (iDCs), thus limiting inflammation and inappropriate T-lymphocyte tolerization. In a previous study, we have reported that NK cells from acute myeloid leukemia patients (AML-NK cells) have deficient natural cytotoxicity receptor (NCR) expression. Herein, we analyzed the consequences of such a defect regarding the regulatory role of AML-NK cells in DC physiology. We show that NK cells display poor cytolytic capacities against DCs derived from healthy donor monocytes or derived from autologous leukemic blasts. These data point to a novel defect in the regulation of adaptive immune responses initiated by DCs in AML patients. This may lead to specific T-lymphocyte tolerization by spontaneous or ex vivo expanded iDCs expressing leukemia-derived antigens. (Blood. 2005;106: 2186-2188)


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DC therapy? Let the natural killer answer
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