My major scientific interest is T cell immunology, specifically the mechanisms that regulate immune T cell activity in a tumor microenvironment. My scientific works are mainly focused on the biology of T cells: from their activation and proliferation in response to virus infection to their differentiation and survival in a tumor microenvironment. In the tumor context, infiltrating effector T (Teff) cells regulate or reject cancer cells while infiltrating regulatory T (Treg) cells suppress the immune responses elicited by Teff and promote tumor progression. 

Efforts to eliminate regulatory Treg cells in cancer patients in order to unleash Teff responses have so far not produced encouraging results...

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My major scientific interest is T cell immunology, specifically the mechanisms that regulate immune T cell activity in a tumor microenvironment. My scientific works are mainly focused on the biology of T cells: from their activation and proliferation in response to virus infection to their differentiation and survival in a tumor microenvironment. In the tumor context, infiltrating effector T (Teff) cells regulate or reject cancer cells while infiltrating regulatory T (Treg) cells suppress the immune responses elicited by Teff and promote tumor progression. 

Efforts to eliminate regulatory Treg cells in cancer patients in order to unleash Teff responses have so far not produced encouraging results. Targeting T cell receptor (TCR) signaling components that regulate intratumoral Treg activation, proliferation and function represents an alternative approach to destabilize Treg and control tumor (Di Pilato et al., Nature 2019).

My career goal is to develop a robust and independent research program at the University of Texas M.D. Anderson Cancer Center. My short and medium-term research goals will be focused on innovative approaches that regulate Treg cells reprogramming and infiltration in cancer.

Specifically, my objectives will be:

1. Determine how antigen presenting cells (APC) directly influence Treg destabilization and if this reprogramming process is related to Treg metabolic switch.
2. Define which chemokine receptors and ligands are involved in the accumulation and survival of Treg on those tumor microenvironments that need robust Treg destabilization to be sensitive to checkpoint blockade therapy.

Accordingly, my long-term goal will be to use these strategies to develop alternative immunotherapy approaches in future clinical trials and to increase the amount of cancer patients that will be responsive to immune checkpoint blockade inhibitors.

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