Journal
BLOOD
Volume 118, Issue 12, Pages 3347-3349Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2011-05-351411
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Funding
- National Institutes of Health [P50 CA97274, R01 CA137198]
- Leukemia & Lymphoma Society
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Natural killer (NK) cell-mediated antibody-dependent cellular cytotoxicity involving Fc gamma RIIIa (CD16) likely contributes to the clinical efficacy of rituximab. To assess the in vivo effects of CD16 polymorphisms on rituximab-induced NK activation, blood was evaluated before and 4 hours after initiation of the initial dose of rituximab in 21 lymphoma subjects. Rituximab induced NK activation and a drop in circulating NK-cell percentage in subjects with the high-affinity [158(VF/VV)] but not the low-affinity [158(FF)] CD16 polymorphism. There was no correlation between NK-cell activation or NK-cell percentage and polymorphisms in CD32A, C1q, or CH50. We conclude that NK activation occurs within 4 hours of rituximab infusion in subjects with the high-affinity CD16 polymorphism but not those with the low-affinity CD16 polymorphism. This finding may help explain the superior clinical outcome seen in the subset of high-affinity CD16 polymorphism lymphoma patients treated with single-agent rituximab. (Blood. 2011;118(12):3347-3349)
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