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Prepublished online as a Blood First Edition Paper on January 23, 2003; DOI 10.1182/blood-2002-10-3030. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-10-3030v1 101/11/4472    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Flynn, S. Articles by Stockinger, B. Search for Related Content PubMed PubMed Citation Articles by Flynn, S. Articles by Stockinger, B. Related Collections Immunobiology Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 June 2003, Vol. 101, No. 11, pp. 4472-4478 IMMUNOBIOLOGY Tumor and CD4 T-cell interactions: tumor escape as result of reciprocal inactivation Sarah Flynn, and Brigitta Stockinger From the Division of Molecular Immunology, National Institute for Medical Research, Mill Hill, London, United Kingdom. This paper addresses the capacity of naive, effector, and memory CD4 T cells to control growth of a major histocompatibility complex (MHC) class II—positive B-cell lymphoma in vivo. To assess the role of T cells on their own without contributions by B cells, antibodies, or natural killer (NK) cells, we generated pure effector or memory CD4 T cells in Rag–/–gc–/– mice deficient in endogenous lymphocytes and NK cells. Lymphoma cells expressing a model antigen were injected into mice with T cells of cognate specificity that were either naive or in effector or resting memory state. Naive T cells were unable to prevent tumor growth, probably due to delay of efficient cross-presentation by dendritic cells. However, both effector and memory T cells, dependent on the amount of antigen available, controlled the tumor for a considerable period of time without the need for dendritic cell stimulation. Nevertheless, the tumor eventually grew uncontrolled in all cases. This was not because of a defect in T-cell homing to the tumor site or loss of MHC class II or costimulatory molecules by the tumor, but reflected mutual paralysis of T-cell responsiveness and antigen processing by tumor cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Perez-Diez, N. T. Joncker, K. Choi, W. F. N. Chan, C. C. Anderson, O. Lantz, and P. Matzinger CD4 cells can be more efficient at tumor rejection than CD8 cells Blood, June 15, 2007; 109(12): 5346 - 5354. [Abstract] [Full Text] [PDF] J. A. Westwood, J. M. Kelly, J. E. Tanner, M. H. Kershaw, M. J. Smyth, and Y. Hayakawa Cutting Edge: Novel Priming of Tumor-Specific Immunity by NKG2D-Triggered NK Cell-Mediated Tumor Rejection and Th1-Independent CD4+ T Cell Pathway J. Immunol., January 15, 2004; 172(2): 757 - 761. [Abstract] [Full Text] [PDF]

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