The present disclosure relates to an anti-WT-1/HLA/A2 antibody with enhanced antibody dependent cell-mediated cytotoxicity (ADCC) function due to altered Fc glycosylation. The antibody, which has reduced fucose and/or galactose, was compared to its normally glycosylated counterpart in binding assays, in vitro ADCC assays, and mesothelioma and leukemia therapeutic models and pharmacokinetic studies in mice. The antibody with normal glycosylation mediated ADCC against hematopoietic and solid tumor cells at concentrations below 1 μg/ml, but the reduced fucosylated antibody was about 5-10 fold more potent in vitro against multiple cancer cell lines, was more potent in vivo against JMN mesothelioma, and effective against SET2 AML and fresh ALL xenografts. ESKM had a shortened half-life (4.9 vs 6.5 days), but an identical biodistribution pattern in C57BL6/J mice. At therapeutic doses of ESKM, there was no difference in half-life or biodistribution in HLA-A2.1 + transgenic mice compared to the parent strain. Importantly, therapeutic doses of ESKM in these mice caused no depletion of total WBCs or hematopoetic stem cells, or pathologic tissue damage.La présente invention concerne un anticorps anti-WT-1/HLA/A2 possédant une fonction de cytotoxicité à médiation cellulaire dépendante de lanticorps (ADCC) renforcée due à une altération de la glycosylation Fc. Lanticorps, comprenant moins de fucose et/ou de galactose, a été comparé à son homologue glycosylé normalement dans des essais de liaison, des dosages ADCC in vitro, des modèles thérapeutiques du mésothéliome et de la leucémie et des études de pharmacocinétique chez la souris. Lanticorps à glycosylation normale a induit une ADCC contre des cellules tumorales hématopoiétiques et solides à des concentrations inférieures à 1 μg/ml, mais lanticorps moins fucosylé sest montré 5 à 10 fois plus puissant in vitro contre plusieurs lignées de cellules cancéreuses, sest montré plus puissant in vivo envers le mésothéliome JMN et sest
