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-Dependent Tumor Rejection1
* National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China; and
Institute of Immunology, Campus Benjamin Franklin, Charite, Berlin, Germany
Though the importance of IFN-
in tumor immunity has been well-demonstrated, little is known about its source and how it is induced. By using various bone marrow chimeric mice, we show here that IFN- essential for tumor immunity is solely produced by hemopoietic cells. Surprisingly, IFN- derived from T cells was not necessary for tumor immunity in this model. In the immunized mice, in which only innate immune cells have the IFN--producing potential, tumors were efficiently rejected. The innate immune cells, such as NK1.1+ cells and CD11b+ cells, can provide sufficient amounts of IFN- which requires, however, the help of T cells. The close cooperation between T cells and innate immune cells during tumor regression is likely mediated by IL-2. Together, our results clearly illustrate how T cells cooperate with innate immune cells for IFN--mediated tumor rejection and this may have important indications for clinical trials of tumor immunotherapy.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by grants of the Chinese Academy of Sciences (to Z.Q.), the National Natural Science Foundation of China (30471571, 30530330), the Ministry of Science and Technology of China (863-2006AA02Z4B9, 973-2006CB504304, and 2006CB910901), and Deutsche Forschungsgemeinschaft (SFB506, R1).
2 Address correspondence and reprint requests to Dr. Zhihai Qin, Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, Chaoyang District, Beijing 100101, China. E-mail address: zhihai{at}ibp.ac.cn
3 Abbreviations used in this paper: BM, bone marrow; D-PBS, Dulbecco’s PBS.
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