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Blood, 1 June 2005, Vol. 105, No. 11, pp. 4399-4406.
Prepublished online as a Blood First Edition Paper on February 3, 2005; DOI 10.1182/blood-2004-10-3854.
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IMMUNOBIOLOGY
Induction of tumor NK-cell immunity by anti-CD69 antibody therapy
Enric Esplugues,
Javier Vega-Ramos,
David Cartoixà,
Berta N. Vazquez,
Ignasi Salaet,
Pablo Engel, and
Pilar Lauzurica
From the Departamento de Fisiología, Universidad de Barcelona, Spain; and Immunology Unit, Department of Cellular Biology and Pathology, Medical School, Institut d'Investigacions Biomediques August Pi i Sunyer, Barcelona, Spain.
The leukocyte activation marker CD69 is a novel regulator of the immune response, modulating the production of cytokines including transforming growth factor- (TGF-). We have generated an antimurine CD69 monoclonal antibody (mAb), CD69.2.2, which down-regulates CD69 expression in vivo but does not deplete CD69-expressing cells. Therapeutic administration of CD69.2.2 to wild-type mice induces significant natural killer (NK) cell–dependent antitumor responses to major histocompatibility complex (MHC) class I low RMA-S lymphomas and to RM-1 prostatic carcinoma lung metastases. These in vivo antitumor responses are comparable to those seen in CD69-/- mice. Enhanced host NK cytotoxic activity correlates with a reduction in NK-cell TGF- production and is independent of tumor priming. In vitro studies demonstrate the novel ability of anti-CD69 mAbs to activate resting NK cells in an Fc receptor–independent manner, resulting in a substantial increase in both NK-cell cytolytic activity and interferon  (IFN) production. Modulation of the innate immune system with monoclonal antibodies to host CD69 thus provides a novel means to antagonize tumor growth and metastasis.
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