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Blood, 15 May 2002, Vol. 99, No. 10, pp. 3661-3667
IMMUNOBIOLOGY
Defective expression and function of natural killer
cell-triggering receptors in patients with acute myeloid
leukemia
Régis T. Costello,
Simona Sivori,
Emanuela Marcenaro,
Marina Lafage-Pochitaloff,
Marie-Joelle Mozziconacci,
Denis Reviron,
Jean-Albert Gastaut,
Daniela Pende,
Daniel Olive, and
Alessandro Moretta
From the Unité d'Immunologie des Tumeurs
Département d'Hématologie, Institut Paoli-Calmettes;
Unité d'Immuno-Génétique, Centre de Transfusion
Sanguine, and Unité INSERM U119, Université de la
Méditerranée, Marseille, France; Laboratorio di Immunologia
Molecolare, Dipartimento di Medicina Sperimentale, Sezione Istologia,
Università degli Studi di Genova, Italy; and U.O. Immunologia,
Istituto Scientifico Tumori, Genova, Italy.
The cytolytic function of natural killer (NK) cells is induced by
the engagement of a series of activating receptors and coreceptors some
of which have recently been identified and collectively termed natural
cytotoxicity receptors (NCRs). Here, we analyzed the cytolytic function
of NK cells obtained from patients with acute myeloid leukemia (AML).
In sharp contrast with healthy donors, in most (16 of 18) patients
with AML the majority of NK cells displayed low NCR surface density
(NCRdull). This phenotype correlated with a weak cytolytic
activity against autologous leukemic cells that could not be reversed
by the monoclonal antibody-mediated disruption of HLA class I/killer
immunoglobulinlike receptor interaction. The remaining 2 patients were
characterized by NK cells having an NCRbright phenotype.
Surprisingly, although displaying NCR-mediated cytolytic activity,
these NCRbright NK cells were unable to kill autologous
leukemic blasts. Importantly, the leukemic blasts from these 2 patients
were also resistant to lysis mediated by normal NCRbright
allogeneic NK cells. Our study suggests that in most instances the
inability of NK cells to kill autologous leukemic blasts is consequent
to low NCR surface expression. In few cases, however, this failure
appears to involve a mechanism of tumor escape based on down-regulation
of ligands relevant for NCR-mediated target cell recognition.
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