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Originally published online as doi:10.1189/jlb.1105628 on January 13, 2006

Published online before print January 13, 2006
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(Journal of Leukocyte Biology. 2006;79:652-662.)
© 2006 by Society for Leukocyte Biology

Effector-phase tolerance: another mechanism of how cancer escapes antitumor immune response

Alan B. Frey1 and Ngozi Monu

Department of Cell Biology and Kaplan Cancer Center, New York University School of Medicine, New York

1Correspondence: Department of Cell Biology, New York University School of Medicine, 550 First Avenue, New York, NY 10016. E-mail: freya01{at}med.nyu.edu

Growth of cancer in rodent models and in patients elicits immune responses directed toward various antigens expressed by the transformed cell. Clearly though, as most tumors grow, unmanipulated antitumor immune responses are incapable of eliminating cancer. Over the past ~15 years, antitumor immunoglobulin and T cells have been used to identify tumor antigens, which in turn, have served as the basis for therapeutic vaccine trials [1 , 2 ]. However, experimental cancer vaccines, although in some patients result in elimination of large tumor burdens, have a low frequency of long-term cancer remission in most patients, ca. <5% [2 ]. Therefore, as tumors express antigens that distinguish themselves from nontransformed cells in immunological terms (i.e., elicit immune responses to growth of primary tumor and can target tumor cells in vivo), and tumor vaccines prime unsuccessful antitumor immune responses in patients, it is likely that growth of cancer induces immune tolerance to tumor cells. Although there are several types of T cell tolerance, mature, antigen-specific CD8+ T cells isolated from tumors are lytic-defective, implying that the tumor microenvironment inactivates the antitumor effector phase. The nature of the functional local tolerance to antitumor immune response is the subject of this review.

Key Words: T cells • cytolysis • tumor




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