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Journal of Virology, February 2007, p. 1313-1318, Vol. 81, No. 3
0022-538X/07/$08.00+0     doi:10.1128/JVI.01943-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Fc{gamma} Receptors Play a Dominant Role in Protective Tumor Immunity against a Virus-Encoded Tumor-Specific Antigen in a Murine Model of Experimental Pulmonary Metastases{triangledown}

Devin B. Lowe,1 Michael H. Shearer,1 Cynthia A. Jumper,1,2,3 Robert K. Bright,1,3 and Ronald C. Kennedy1,3*

Departments of Microbiology and Immunology,1 Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas,2 Southwest Cancer Treatment and Research Center, Lubbock, Texas3

Received 6 September 2006/ Accepted 5 November 2006

Simian virus 40 (SV40) large tumor antigen (Tag) represents a virus-encoded tumor-specific antigen expressed in many types of human cancers and a potential immunologic target for antitumor responses. Fc receptors are important mediators in the regulation and execution of host effector mechanisms against conditions including infectious diseases, autoimmunity, and cancer. By examining tumor protection in SV40 Tag-immunized wild-type BALB/c mice using an experimental pulmonary metastasis model, we attempted to address whether engagement of the immunoglobulin G Fc receptors (Fc{gamma}Rs) on effector cells is necessary to mediate antitumor responses. All immunized BALB/c Fc{gamma}R–/– knockout mice developed anti-SV40 Tag antibody responses prior to experimental challenge with a tumorigenic cell line expressing SV40 Tag. However, all mice deficient in the activating Fc{gamma}RI (CD64) and Fc{gamma}RIII (CD16) were unable to mount protective immunologic responses against tumor challenge and developed tumor lung foci. In contrast, mice lacking the inhibitory receptor Fc{gamma}RII (CD32) demonstrated resistance to tumorigenesis. These results underscore the importance of effector cell populations expressing Fc{gamma}RI/III within this murine tumor model system, and along with the production of a specific humoral immune response, antibody-dependent cell-mediated cytotoxicity (ADCC) may be a functioning mechanism of tumor clearance. Additionally, these data demonstrate the potential utility of ADCC as a viable approach for targeting vaccination strategies that promote Fc{gamma}RI/III scavenging pathways against cancer.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Texas Tech University Health Sciences Center, 3601 4th Street, MS 6591, Lubbock, TX 79430. Phone: (806) 743-2545. Fax: (806) 743-2334. E-mail: ronald.kennedy{at}ttuhsc.edu.

{triangledown} Published ahead of print on 15 November 2006.

Journal of Virology, February 2007, p. 1313-1318, Vol. 81, No. 3
0022-538X/07/$08.00+0     doi:10.1128/JVI.01943-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





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