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Blood, 1 October 2007, Vol. 110, No. 7, pp. 2561-2564.
Prepublished online as a Blood First Edition Paper on May 2, 2007; DOI 10.1182/blood-2007-01-070656.
 Previous Article | Next Article 
Submitted January 30, 2007
Accepted April 23, 2007
Increased natural killer cell expression of CD16, and augmented binding and ADCC activity to rituximab among individuals expressing the Fc RIIIA-158 V/V and V/F polymorphism
Evdoxia Hatjiharissi, Lian Xu, Daniel Ditzel Santos, Zachary R. Hunter, Bryan T Ciccarelli, Sigitas Verselis, Michael Modica, Yang Cao, Robert J. Manning, Xavier Leleu, Elizabeth A. Dimmock, Alexandros Kortsaris, Constantine Mitsiades, Kenneth C. Anderson, Edward A. Fox, and Steven P. Treon*
Bing Center for Waldenstrom's Macroglobulinemia, Dana-Farber Cancer Institute, Boston, MA, United States
Harvard Medical School, Boston, MA, United States
Molecular Diagnostics Laboratory, Dana-Farber Cancer Institute, Boston, MA, United States
School of Medicine, Democritus University of Thrace, Alexandroupolis, Greece
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, Boston, MA, United States
* Corresponding author; email: steven_treon{at}dfci.harvard.edu.
The presence of valine (V) at Fc RIIIa-158 (CD16) is known to improve clinical response to rituximab in indolent non-Hodgkin's lymphoma (NHL). Little is known about the basic mechanisms for this observation. We examined natural killer (NK) cells from healthy donors representing the FcRIIIa-158 polymorphic subgroups (V/V, V/F and F/F) for gene transcript and cell-surface CD16 expression, rituximab binding and rituximab-dependent NK cell-mediated cytotoxicity (ADCC). We observed higher levels of FcRIIIa transcripts among individuals with the FcRIIIa-158 V/V versus -V/F or -F/F genotype (p<0.001); increased cell-surface CD16 expression by quantitative flow cytometry on NK cells from individuals expressing at least one valine at FcRIIIa-158 versus -F/F (p=0.029), as well as augmented rituximab binding and rituximab-dependent ADCC activity. These results suggest that individuals expressing at least one valine at FcRIIIa-158 might, in part, have better clinical outcomes due to increased CD16 expression, rituximab binding, and rituximab-mediated ADCC.
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