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题目:: Enhancement of anti-leukemia activity of NK cells in vitro and in vivo by inhibition of leukemia cell-induced NK cell damage.
作者:: Arriga(Roberto),Caratelli(Sara),Coppola(Andrea),Spagnoli(Giulio Cesare),Venditti(Adriano),Amadori(Sergio),Lanzilli(Giulia),Lauro(Davide),Palomba(Patrizia),Sconocchia(Tommaso),Del Principe(Maria Ilaria),Maurillo(Luca),Buccisano(Francesco),Capuani(Barbara),Ferrone(Soldano),Sconocchia(Giuseppe)
状态:: 发布时间2016-02-16 , 更新时间 2016-10-19
期刊:: Oncotarget
摘要:: Acute myeloid leukemia (AML) cells induce, in vitro, NK cell abnormalities (NKCAs) including apoptosis and activating receptor down-regulation. The potential negative impact of AML cells on the therapeutic efficacy of NK cell-based strategies prompted us to analyze the mechanisms underlying NKCAs and to develop approaches to protect NK cells from NKCAs. NKCA induction by the AML leukemia cells target a subpopulation of peripheral blood NK cells and is interleukin-2 independent but is abrogated by a long-term culture of NK (LTNK) cells at 37°C. LTNK cells displayed a significantly enhanced ability to damage AML cells in vitro and inhibited the subcutaneous growth of ML-2 cells grafted into CB17 SCID mice. Actinomycin D restored the susceptibility of LTNK cells to NKCAs while TAPI-0, a functional analog of the tissue inhibitor of metalloproteinase (TIMP) 3, inhibits ML-2 cell-induced NKCAs suggesting that the generation of NK cell resistance to NKCAs involves RNA transcription and metalloproteinase (MPP) inactivation. This conclusion is supported by the reduced susceptibility to AML cell-induced NKCAs of LTNK cells in which TIMP3 gene and protein are over-expressed. This information may contribute to the rational design of targeted strategies to enhance the efficacy of NK cell-based-immunotherapy of AML with haploidentical NK cells.
语言:: eng
DOI:

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