JUN 18, 2020 9:00 AM PDT

Unveiling the role of T cell dysfunction in the development and progression of glioblastoma

  • Postdoctoral researcher
      My area of expertise is tumour immunology, particularly T cell biology and the generation of memory T cells in non-lymphoid tissues. I did my Ph.D. in Chile at Fundacion Ciencia & Vida studying the role of skin-resident memory CD8 T cells in the immunity against melanoma. My work was one of the first to show the role of tissue-resident memory CD8 T cells in the immunity against tumours. During my Ph.D., I also became interested on skin dendritic cells and their role on T cell memory, area I explored during an internship at Stanford University in the United States. At the end of my Ph.D., I moved to the United Kingdom and start my postdoctoral research at UCL mentored by Professor Sergio Quezada. The question I am currently pursuing is why tumours scape immune surveillance and develop even in the presence of an ongoing immune response. Given that T cells are key players of tumour immunity, whether these cells become dysfunctional losing their ability to destroy cancer cells could be one of the main mechanisms of tumour scape. In this context, glioblastoma appears as a unique opportunity to study T cell dysfunction given its immunosuppressive environment. I am convinced that studying the mechanisms by which glioblastoma makes T cells dysfunctional will give us a clue of unknown regulators of this process that could be used to develop novel immunotherapies.

    DATE:  June 18, 2020
    TIME:   9:00am PDT, 12:00pm EDT
    Despite the success of immunotherapy against several malignancies including melanoma and lung adenocarcinoma, glioblastoma remains the exception. CD8+ T cells are the main drivers of the response to immunotherapy, but most of them differentiate into a dysfunctional state inside the tumour. The signals underpinning CD8+ T cell dysfunction in glioblastoma remain uncharacterized. Using a transplantable mouse model of glioblastoma, we have found a high infiltration of CD4 and CD8 T cells expressing several inhibitory receptors such as PD-1, TIM-3 and LAG-3, suggesting the acquisition of a dysfunctional state. We hypothesize that chronic antigen stimulation through the T cell receptor is driving differentiation and the acquisition of a dysfunctional state on T cells, facilitating tumour progression. The main learning objectives of this talk will be to highlight the relevance of studying brain tumour immunology and to make a brief description of the approach we are using in order to identify and validate potential targets to treat this devastating disease.
    Learning Objectives:
    • Understand the relevance of doing research on brain tumours
    • An overview of the immune landscape of glioblastoma in mouse models;
    • Novel approcches to identify targets for immunotherapy of glioblastoma;
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