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Equilibrium between Host and Cancer Caused by Effector T Cells Killing Tumor Stroma

¹ Department of Pathology and Committee on Immunology, University of Chicago, Chicago, Illinois; ² San Antonio Cancer Institute, University of Texas Health Sciences Center, San Antonio, Texas; ³ Department of Surgery, Medical University of South Carolina, Charleston, South Carolina; and ⁴ Department of Biochemistry, University of Illinois, Urbana, Illinois

Requests for reprints: Bin Zhang, San Antonio Cancer Institute, University of Texas Health Sciences Center, 2040 Babcock Road, Suite 201, San Antonio, TX 78229. Phone: 210-562-5243; Fax: 210-562-5292; E-mail: Zhangb3{at}uthscsa.edu.

Key Words: Equilibrium • T cells • Tumor stroma

The growth of solid tumors depends on tumor stroma. A single adoptive transfer of CD8⁺ CTLs that recognize tumor antigen–loaded stromal cells, but not the cancer cells because of MHC restriction, caused long-term inhibition of tumor growth. T cells persisted and continuously destroyed CD11b⁺ myeloid-derived, F4/80⁺ or Gr1⁺ stromal cells during homeostasis between host and cancer. Using high-affinity T-cell receptor tetramers, we found that both subpopulations of stromal cells captured tumor antigen from surrounding cancer cells. Epitopes on the captured antigen made these cells targets for antigen-specific T cells. These myeloid stromal cells are immunosuppressive, proangiogenic, and phagocytic. Elimination of these myeloid cells allowed T cells to remain active, prevented neovascularization, and prevented tumor resorption so that tumor size remained stationary. These findings show the effectiveness of adoptive CTL therapy directed against tumor stroma and open a new avenue for cancer treatments. [Cancer Res 2008;68(5):1563–71]

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