Tumor-primed natural killer cells from patients with multiple myeloma lyse autologous, NK-resistant, bone marrow-derived malignant plasma cells.

Autor: Katodritou E; Department of Hematology, University College Medical School, London, United Kingdom. eirinikatodritou@gmail.com, Terpos E, North J, Kottaridis P, Verrou E, Gastari V, Chadjiaggelidou C, Sivakumaran S, Jide-Banwo S, Tsirogianni M, Kapetanos D, Zervas K, Lowdell MW
Jazyk: angličtina
Zdroj: American journal of hematology [Am J Hematol] 2011 Dec; Vol. 86 (12), pp. 967-73. Date of Electronic Publication: 2011 Sep 14.
DOI: 10.1002/ajh.22163
Abstrakt: Natural killer (NK) cells are cytotoxic lymphocytes able to kill tumor cells and virus-infected cells. Human-resting NK cells can be activated by co-culture with NK-resistant CTV-1a cells. These tumor-activated cells (TaNKs) are cytotoxic to a range of NK-resistant tumor cells in vitro. This potential, however, has not been explored in multiple myeloma (MM). In this study, we demonstrate that TaNK cells from 21 MM patients lyse a variety of myeloma targets, including primary isolates of autologous and allogeneic CD138+ myeloma cells whilst sparing CD138-ve bone marrow cells. Myeloma patients' TaNK-induced lysis of the U266 cell line was significantly higher compared to normal controls (median-specific lysis 79.1% vs. 69.5%) (P = 0.003). In addition, TaNKs induced substantial lysis of autologous and allogeneic CD138+ myeloma cells (median-specific lysis 52.5% and 37.4%, respectively). The percentage of specific lysis did not correlate with important disease characteristics (ISS, age, and high-risk molecular abnormalities) or with the disease status and antimyeloma treatment, including novel agents and dexamethasone. In conclusion, tumor-primed NK cells are able to induce substantial lysis of myeloma targets including autologous and allogeneic CD138+ myeloma plasma cells and could be an additional therapeutic approach in MM, particularly in the era of novel agents.
(Copyright © 2011 Wiley-Liss, Inc.)
Databáze: MEDLINE
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