Abstract:
:Natural killer T (NKT) cells with an invariant T-cell receptor for alpha-galactosylceramide (alphaGalCer) that is presented by CD1d have been reported to be cytotoxic for myelomonocytic leukemia cells. However, the necessity for leukemia cell CD1d expression, the role of alphaGalCer, and the cytotoxic mechanisms have not been fully elucidated. We evaluated these issues with myeloid leukemia cells from 14 patients and purified NKT cells that were alphaGalCer/CD1d reactive. CD1d was expressed by 80-100% of cells in three of seven acute myeloid leukemias (AMLs) and by 28-77% of cells in five of six juvenile myelomonocytic leukemias (JMML). CD1d+ AML cells were myelomonocytic or monoblastic types, and CD1d+ JMML cells were differentiated and CD34-. Cytotoxicity required leukemia cell CD1d expression and was increased by alphaGalCer (P<0.0001) and inhibited by anti-CD1d mAb (P<0.001). The perforin/granzyme-B pathway of NKT cells caused up to 85% of cytotoxicity, and TNF-alpha, FASL, and TRAIL mediated additional killing. CD56+ NKT cells expressed greater perforin and were more cytotoxic than CD56 NKT cells without alphaGalCer (P<0.0001), but both subpopulations were highly and equally cytotoxic in the presence of alphaGalCer. We conclude that CD1d expression is stage-specific for myelomonocytic leukemias and could provide a target for NKT-cell-mediated immunotherapy.
journal_name
Leukemiajournal_title
Leukemiaauthors
Metelitsa LS,Weinberg KI,Emanuel PD,Seeger RCdoi
10.1038/sj.leu.2402943subject
Has Abstractpub_date
2003-06-01 00:00:00pages
1068-77issue
6eissn
0887-6924issn
1476-5551pii
2402943journal_volume
17pub_type
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