In addition to immune checkpoint pathways—such as CTLA-4 and PD-1/PD-L1—that can suppress immune activity, T cells have activation receptors that are necessary to stimulate T cells against tumors. Therefore, Dr. Ludovic Martinet is investigating how the potential loss of one such activation receptor—CD226—might impact T cell dysfunction and the effectiveness of immunotherapy as well as whether it could serve as a useful biomarker for helping doctors predict patient responses.
By analyzing the interplay between T cell receptor activity and CD226 signaling, Martinet aims to provide the molecular basis underlying the critical role of CD226 in killer T cell activation. Additionally, using mouse models of cancer as well as comparisons with patient samples, he will seek to uncover evidence that CD226’s absence promotes cancer immune escape and alters responses to cancer immunotherapy. Overall, the insights he uncovers may lead to a paradigm shift concerning the mechanisms that can drive T cell dysfunction and promote resistance to immunotherapy, and ultimately help identify new biological markers that could be used to improve treatment strategies in the clinic.
Projects and Grants
Harnessing CD8+ T Cell antitumor responses by manipulating extracellular ATP signaling
Institut National de la Santé et de La Recherche Médicale (INSERM, France) | All Cancers | 2020
Let's spread the word about Immunotherapy! Click to share this page with your community.