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Critical Reviews™ in Immunology
IF: 1.352 5-Year IF: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN Print: 1040-8401
ISSN Online: 2162-6472

Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v18.i1-2.60
pages 47-54

Strategies for Tumor Elimination by Cytotoxic T Lymphocytes

Linda A. Sherman
Department of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA
Matthias Theobald
Johannes Gutenberg University, Langenbeck str. 1, Mainz, Germany
David Morgan
Department of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA
Javier Hernandez
Department of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA
Igor Bacik
Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD
Jonathan Yewdell
Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD
Jack Bennink
Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD
Judith Biggs
Department of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA

ABSTRACT

Despite differences in their tissue of origin, many tumors share high level expression of certain tumor-associated proteins. Our laboratory has focused on the possibility of utilizing antigenic components of these proteins as a focus for T-cell immunotherapy of cancer. The advantage of targeting such commonly expressed proteins is the fact that such therapy could be of value in eliminating many different types of tumors. A potential barrier in the identification of T-cell epitopes derived from these proteins and presented by tumor cells is the fact that these proteins are also expressed at low levels in some normal tissues, and therefore, self-tolerance may eliminate T cells that are capable of recognizing these epitopes with high avidity. We have utilized two different murine model systems to explore the extent to which self-tolerance may limit the immune response to a tumor-specific antigen. The first compared the ability of mice deficient in expression of murine p53 (p53 knock-out mice) and normal mice, to respond against several epitopes of the p53 protein. The second model compares the ability of conventional mice with transgenic mice that express the influenza hemagglutinin in the periphery to respond to a dominant antigenic peptide of this transgene product. In both models we have investigated the effect self-tolerance has on elimination of tumors expressing the toleragen.


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