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.
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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