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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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Submitted March 29, 2005
Accepted May 22, 2005
Defective killing of dendritic cells by autologous natural killer cells from acute myeloid leukemia patients
Cyril Fauriat, Alessandro Moretta, Daniel Olive, and Regis T Costello*
Laboratoire d'Immunologie des Tumeurs, Institut Paoli-Calmettes, Marseille, France
Dipartimento di Medicina Sperimentale, Sezione di Istologia, Universita degli Studi di Genova, Genova, Italy
Laboratoire d'Immunologie des Tumeurs, Institut Paoli-Calmettes, Marseille, France; Faculte de Medecine de Marseille, Marseille, France
Laboratoire d'Immunologie des Tumeurs, Institut Paoli-Calmettes, Marseille, France; Faculte de Medecine de Marseille, Marseille, France; Departement d'Hematologie, Institut Paoli-Calmettes, Marseille, France
* Corresponding author; email: regis.costello{at}free.fr.
At the frontier between innate and adaptive immunity, dendritic cells (DC) secrete numerous cytokines and express co-stimulatory molecules that initiate or enhance natural killer (NK) and T lymphocyte responses. NK cells also regulate DC physiology by killing immature DC (iDC), thus limiting inflammation and inappropriate T-lymphocyte tolerization. In a previous study, we have reported that NK from acute myeloid leukemia patients (AML-NK) have deficient natural cytotoxicity receptor (NCR) expression. Herein, we analyzed the consequences of such a defect regarding the regulatory role of AML-NK in DC physiology. We show that NK cells display poor cytolytic capacities against DC derived from healthy donors monocytes or derived from autologous leukemic blasts. These data point to a novel defect in the regulation of adaptive immune responses initiated by DC in AML patients. This may lead to specific T-lymphocyte tolerization by spontaneous or ex vivo expanded iDC expressing leukemia-derived antigens.
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