Mauro Di Pilato
Assistant Professor
The University of Texas MD Anderson Cancer Center
Department of Immunology
In cancer immunotherapy, many studies focus on the induction and activation of effector CD8 T cells as suitable strategies to reject tumors. Dendritic cells (DC) and neutrophils (Neu) also participate in the control of tumor progression by cross-talking with T cells, while regulatory T (Treg) cells play a major role in dampening CD8 T cell activity and promote tumor growth.
Poorly T cell infiltrated melanomas remain a big challenge in cancer immunotherapy. Indeed, those patients do not respond to the current treatments in clinical trials. Recently, many studies focus on mouse Treg instability and their gain of effector activity as an alternative immunotherapy approach to cure cancer.
What is needed for unstable Treg to accumulate in the tumor microenvironment is still unknown. Thus, it is important to define which DC and Neu subsets are required for Treg to expand on tumors. It is currently not known whether unstable Treg accumulate within specific intratumoral niches and which immune signals of intratumoral accumulation they do receive in those areas.
Therefore, we would like to investigate and characterize which immune signals are involved in the intratumoral infiltration of unstable Treg. Specifically, we want to focus on pathways that are involved in Treg intratumoral destabilization, proliferation and survival and define new strategies of Treg accumulation. Our goal is to develop new approaches that will increase the effectiveness of cancer immunotherapy and the number of cancer patients who will respond to immune checkpoint blockade inhibitors, and finally to prevent the progression of primary melanomas.
NCBI Bibliography
MDACC Faculty
Education & Training
PhD, Autonomous University of Madrid, 2015