Eliciting Autoimmunity to Ovarian Tumors in Mice by Genetic Disruption of T Cell Tolerance Mechanisms

Abstract

We are developing a mouse model for ovarian cancer that will allow monitoring of the in vivo activities of tumor-specific T cell clones as they encounter ovarian tumors in vivo. We propose to "tag" the neu oncogene with two identified T cell epitopes so as to confer recognition by available T cell receptor (TCR) transgenic T cells. When expressed in the murine ovarian tumor cell line IDS, epitope-tagged neu (designated neuo(Tl/0T2) should induce formation of aggressive ovarian adenocarcinomas that express the epitope tags and hence are recognizable by adoptively transferred TCR transgenic T cells. We successfully made the neuo Tl/0T2 expression construct, but found it to be overly immunogenic in vivo such that tumors were spontaneously rejected. Therefore, we derived a third generation 1D8 tumor cell line that has a shorter tumor latency and decreased expression of MHC Class I, which should make it less immunogenic. Meanwhile, we have commenced adoptive T cell transfer experiments using a convenient, transplantable lymphoma model. With this model, we are investigating the phenomenon of antigen spreading that results after adoptive transfer of tumor-specific T cells. Finally, Cbl-b -/- mice have been obtained and are currently being backcrossed onto the B6 background for Aim 3.

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Document Details

Document Type
Technical Report
Publication Date
Aug 01, 2003
Accession Number
ADA421153

Entities

People

  • Brad H Nelson

Tags

DTIC Thesaurus Topics

  • Autoimmune Diseases
  • Autoimmunity
  • Biomedical Research
  • Blood
  • British Columbia
  • Cancer
  • Cell Line
  • Cells
  • Clones
  • Demographic Cohorts
  • Department Of Defense
  • Immune System Phenomena
  • Immunity
  • Lymphocytes
  • Neoplasms
  • Ovarian Cancer
  • Tumor Cell Line

Fields of Study

  • Biology

Readers

  • Immunology
  • Oncology (Cancer Research).

Technology Areas

  • Biotechnology
  • Biotechnology - Cancer Biotech