HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hollenbaugh, J. A. Articles by Dutton, R. W. Search for Related Content PubMed PubMed Citation Articles by Hollenbaugh, J. A. Articles by Dutton, R. W.

The Rate of the CD8-Dependent Initial Reduction in Tumor Volume Is Not Limited by Contact-Dependent Perforin, Fas Ligand, or TNF-Mediated Cytolysis¹

Joseph A. Hollenbaugh^*,, Joyce Reome^*, Mark Dobrzanski^* and Richard W. Dutton^2,*

^* Trudeau Institute, Saranac Lake, NY 12983; and Cell and Molecular Biology Program, University of Vermont, Burlington, VT 05405

Established EG7 tumors expressing OVA and growing at an intradermal site become rapidly reduced in size following adoptive therapy with in vitro-generated type I CD8 T cell (Tc1) effectors generated from naive CD8 T cells from transgenic TCR OVA-specific mice. Tc1 effectors kill EG7 target cells in vitro by a perforin-dependent mechanism. However, we show that there is no quantitative diminution of the initial phase of antitumor activity in vivo, whether the Tc1 effectors are derived from perforin-, Fas ligand-, or TNF-deficient transgenic TCR mice or whether the recipients are perforin deficient. Tumors are also equally well controlled whether the Tc1 effectors come from mice deficient in perforin plus Fas ligand or perforin plus TNF. Control of tumor growth is diminished when Tc1 effectors generated from IFN--deficient mice are used. We conclude that control of tumor growth is not in any way affected by loss of contact-mediated lytic mechanisms, and conclude that the CD8 effectors must act by recruiting host effector mechanisms to control tumor growth.

This article has been cited by other articles:

				J. M. Curtsinger, M. Y. Gerner, D. C. Lins, and M. F. Mescher Signal 3 Availability Limits the CD8 T Cell Response to a Solid Tumor J. Immunol., June 1, 2007; 178(11): 6752 - 6760. [Abstract] [Full Text] [PDF]

				A. Boissonnas, L. Fetler, I. S. Zeelenberg, S. Hugues, and S. Amigorena In vivo imaging of cytotoxic T cell infiltration and elimination of a solid tumor J. Exp. Med., February 19, 2007; 204(2): 345 - 356. [Abstract] [Full Text] [PDF]

				J. A. Hollenbaugh and R. W. Dutton IFN-{gamma} Regulates Donor CD8 T Cell Expansion, Migration, and Leads to Apoptosis of Cells of a Solid Tumor. J. Immunol., September 1, 2006; 177(5): 3004 - 3011. [Abstract] [Full Text] [PDF]

				M. D McKenzie, N. L Dudek, L. Mariana, M. M. Chong, J. A Trapani, T. W. Kay, and H. E Thomas Perforin and Fas induced by IFN{gamma} and TNF{alpha} mediate beta cell death by OT-I CTL Int. Immunol., June 1, 2006; 18(6): 837 - 846. [Abstract] [Full Text] [PDF]

				A. Song, X. Tang, K. M. Harms, and M. Croft OX40 and Bcl-xL Promote the Persistence of CD8 T Cells to Recall Tumor-Associated Antigen J. Immunol., September 15, 2005; 175(6): 3534 - 3541. [Abstract] [Full Text] [PDF]