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Blood, 16 April 2009, Vol. 113, No. 16, pp. 3809-3812. Prepublished online as a Blood First Edition Paper on February 4, 2009; DOI 10.1182/blood-2008-10-185280.
Submitted October 20, 2008
James P. Wilmot Cancer Center, University of Rochester School of Medicine and Dentistry, Rochester, NY, United States * Corresponding author; email: steven_bernstein{at}urmc.rochester.edu.
The incorporation of rituximab, a chimeric anti-CD20 monoclonal antibody, into the therapeutic armamentarium for patients with follicular lymphoma (FL) has significantly improved treatment outcome for such patients. Despite the almost universal application of this therapy however, its exact mechanism of action has not been completely defined. One proposed mechanism is that of a "vaccinal effect", whereby FL cell kill by rituximab results in the elicitation of a FL specific T-cell response. The demonstration that rituximab can even elicit such a response in patients, has to our knowledge, never been shown. We analyzed the response against the immunoglobulin expressed by the FL before and after rituximab monotherapy in five FL patients and found an increase in FL idiotype specific T-cells post-rituximab in 4/5 patients. Our data thus provide "proof of principle" for the ability of passive immunotherapy with rituximab to elicit an active FL specific cellular response.
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