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Eduardo Sotomayor
Professor

Contact

Office:
Phone: 813/745-1385
Email: Eduardo.Sotomayor@moffitt.org

Education

M.D.: Federico Villarreal National, University School of Medicine; Lima, Peru, 1988.
Postdoctoral Fellow: Department of Microbiology and Immunology, University of Miami School of Medicine (Mentor: Diana M. Lopez Ph.D.), 1989-1992.
Internship: Jackson Memorial Medical Center, University of Miami School of Medicine (Internal Medicine), 1992-1993.
Residency: Jackson Memorial Medical Center, University of Miami School of Medicine (Internal Medicine), 1993-1995.
Fellowship in Oncology: Johns Hopkins Oncology Center (Mentor: Hyam Levitsky, M.D.), 1995-1998.

Research

The immune system is well-equipped with cells that, when appropriately stimulated, can specifically recognize and kill cancer cells. However, as tumors expand a progressive impairment in the function of immune cells has been described. This impairment of T- cells negatively affects the ability of these cells to respond to immune-enhancing strategies currently used in the treatment of malignancies (i.e. vaccination with tumor-cell based vaccines). Indeed, studies in our laboratory have shown that early during tumor development (either hematologic malignancies or solid tumors), a critical subset of cells of the immune system (CD4+ T cells) are "paralyzed" or rendered tolerant. In other words, antigen-specific T-cells are still present in the tumor-bearing host but are unable to respond to stimulation that otherwise would lead to an effective activation of these cells.

Therefore, in our lab we have two major areas of interest:
a) To understand the cellular and molecular mechanism(s) involved in tolerance induction
In this regard, using parent-into-F1 bone marrow chimeras we have unambiguously demonstrated that tumor antigen processing and presentation by host's antigen-presenting cells or APCs (not tumor cell themselves) is the dominant mechanism underlying the development of antigen-specific T-cell tolerance. The requirement, therefore, for APCs in the induction of immune tolerance together with their well known role in priming effective T-cell responses, places APCs at the center of a critical decision leading to T-cell priming versus tolerance. More recently, we have identified that the JAK-STAT3 pathway in APCs may be playing a role in this critical decision.
b) Design strategies aimed to prevent and or revert this unresponsive state and therefore enhance the efficacy of the current generation of immunotherapeutic strategies.
We are currently exploring whether strategies designed to enhance APCs function (aminobisphosphonates) or strategies aimed to activate novel costimulatory pathways (CD40-CD40L; OX40R-OX40L; 4-1BBL/4-1BB) or to block inhibitory pathways (CTLA4 blockade; CD30-CD30L blockade) may prevent and or revert tumor induced antigen-specific T cell tolerance.