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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. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2007-01-070656v1 110/7/2561    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Hatjiharissi, E. Articles by Treon, S. P. Search for Related Content PubMed PubMed Citation Articles by Hatjiharissi, E. Articles by Treon, S. P. Related Collections Immunobiology Immunotherapy Brief Reports Clinical Trials and Observations Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Brief Report Increased natural killer cell expression of CD16, augmented binding and ADCC activity to rituximab among individuals expressing the FcRIIIa-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 FcRllla (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 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. We observed higher levels of FcRIIIa transcripts among individuals with the FcRIIIa-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 FcRIIIa-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 FcRIIIa-158 might, in part, have better clinical outcomes due to increased CD16 expression, rituximab binding, and rituximab-mediated ADCC. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: FcRIIIa role in rituximab efficacy Julie M. Roda and John C. Byrd Blood 2007 110: 2220. 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