STAT6 Deletion Enhances Immunity to Mammary Carcinoma
Abstract
The Stat6 (signal transducer activator of transcription) gene is essential for the production of IL-4 and IL-13, two cytokines that govern the activation of CD4+ T helper type 2 (Th2) cells. We hypothesized that mice with a deleted Stat6 gene (Stat6-/-) would have enhanced tumor immunity because they would preferentially make tumor-reactive Th1 cells, which are thought to facilitate the activation of CD8+ cytotoxic T cells (Tc), thereby improving tumor-specific immune responses. Our preliminary results demonstrate that tumor immunity to a metastatic mammary carcinoma is enhanced in the absence of the Stat6 gene. Although additional experiments demonstrated that tumor rejection in Stat6* mice is immunologically mediated by CD8+ T lymphocytes, this effect is not due to an improved this response. Therefore, elimination of the Stat6 gene is a potent strategy for enhancing rejection of mammary cancer cells; however, the mechanistic explanation for the improved tumor immunity is not clear. The purpose of this project is to determine the potency of the Stat6 effect for enhancing immunity to metastatic mammary carcinoma, and to identify the mechanism underlying the improved immunity. These experiments will not only provide insight into regulation of anti-tumor immunity, but may also suggest novel approaches for enhancing anti-tumor immune responses.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2003
- Accession Number
- ADA427169
Entities
People
- Suzanne Ostrand-Rosenberg
Organizations
- University of Maryland, Baltimore