Understanding the interactions between tumor cells and the immune system is of interest not only for elucidating cancer mechanisms but also for immunotherapy of cancer. Since tumors are derived from normal self tissues, the default pathway to tumor antigens is likely tolerance. Therefore, it will be essential to remove the self-tolerance checkpoints to enhance tumor immunity. Using various tumor models, we are investigating:
- Is inhibition of TGF-beta signaling in T cells sufficient to induce immunity to spontaneous tumors? If so,
- What are the effector mechanisms utilized by T cells to prevent cancer progression?
- What are the functions of TGF-beta1 produced by tumor cells and various immune cell types in regulating T cell responses to tumors?
- Can the TGF-beta pathway in T cells be targeted for the immunotherapy of cancer?
Obviously tumors are altered self, and they possess characteristics resembling infectious agents such as unbridled proliferation, induction of tissue damage, and the life-threatening feature of dissemination (metastasis). The interactions between tumor cells and the immune system remain poorly understood. The laboratory is interested in developing novel mouse tumor models to explore such interactions in vivo. The questions that we are addressing include:
- Does the innate and/or adaptive immune system mount immune responses to spontaneous tumors?
- What are the functions of immune effector pathways in regulating cancer progression?
