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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.

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IMMUNOBIOLOGY

Brief Report

Increased natural killer cell expression of CD16, augmented binding and ADCC activity to rituximab among individuals expressing the Fc{gamma}RIIIa-158 V/V and V/F polymorphism

Evdoxia Hatjiharissi1,3, Lian Xu1, Daniel Ditzel Santos1,2, Zachary R. Hunter1, Bryan T. Ciccarelli1, Sigitas Verselis2,4, Michael Modica2,4, Yang Cao1, Robert J. Manning1, Xavier Leleu1,2, Elizabeth A. Dimmock1, Alexandros Kortsaris3, Constantine Mitsiades2,5, Kenneth C. Anderson2,5, Edward A. Fox2,4, and Steven P. Treon1,2

1 Bing Center for Waldenstrom's Macroglobulinemia, Dana-Farber Cancer Institute, Boston, MA; 2 Harvard Medical School, Boston, MA; 3 School of Medicine, Democritus University of Thrace, Alexandroupolis, Greece; 4 Molecular Diagnostics Laboratory, Dana-Farber Cancer Institute, Boston, MA; and 5 Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, Boston, MA

The presence of valine (V) at position 158 of Fc{gamma}Rllla (CD16) is known to improve clinical response to rituximab in indolent non-Hodgkin lymphoma (NHL). Little is known about the basic mechanisms for this observation. We examined natural killer (NK) cells from healthy donors representing the Fc{gamma}RIIIa-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. We observed higher levels of Fc{gamma}RIIIa transcripts among individuals with the Fc{gamma}RIIIa-158 V/V versus V/F or F/F genotype (P < .001); increased cell surface CD16 expression by quantitative flow cytometry on NK cells from individuals expressing at least one valine at Fc{gamma}RIIIa-158 versus F/F (P = .029); as well as augmented rituximab binding and rituximab-mediated, antibody-dependent cellular cytotoxicity (ADCC). These results suggest that individuals expressing at least one valine at Fc{gamma}RIIIa-158 might, in part, have better clinical outcomes due to increased CD16 expression, rituximab binding, and rituximab-mediated ADCC.


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Fc{gamma}RIIIa role in rituximab efficacy
Julie M. Roda and John C. Byrd
Blood 2007 110: 2220. [Full Text] [PDF]



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