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Published online before print November 29, 2004
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Article |
,
,
,
Departments of *Pathology,
Medicine, and
Radiation Oncology, and the New York University Cancer Institute, New York University School of Medicine, New York; and
Children’s National Medical Center, Center for Cancer and Immunology, Washington, District of Columbia
@ To whom correspondence should be addressed. E-mail: demars01{at}med.nyu.edu.
| Abstract |
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Dendritic cells (DC) play a crucial role in initiating immune responses to tumors. DC can efficiently present antigens from apoptotic tumor cells, but apoptotic cells are thought to lack the inflammatory signals required to induce DC maturation. Here, we show that apoptosis of 67NR mouse carcinoma cells via the Fas (CD95) pathway or induced by the anticancer drug bortezomib (PS-341) but not by ultraviolet irradiation is associated with the production of maturation signals for DC. These data have important implications for the effects of chemotherapy on antitumor immunity in solid and hematologic malignancies.
Key Words: costimulation tumor immunity Fas/CD95 chemotherapy
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