Michel J.P. DuPage

This study shows that MHCII+ cancer-associated fibroblasts (CAFs) in pancreatic cancer can promote antitumor immunity through IFNγ-driven mechanisms, counteracting Treg suppression.

This study improves cross-presentation by using fusion-dependent mini-proteins to enhance antigen delivery to the dendritic cell cytosol, leading to better MHC-I presentation and T-cell activation.

This study shows that Listeria monocytogenes evades MAIT cells by lacking riboflavin biosynthesis, and engineered strains that produce riboflavin activate MAIT cells, offering therapeutic potential against infections and cancer.

Intra-tumoral Treg ablation enhances NK cell-mediated tumor control by restoring IL-2 production, effective against both MHC I+ and MHC I- cancers without systemic toxicity.

This study shows targeting FSP1 in regulatory T cells disrupts their immunosuppression, enhancing anti-tumor immunity without causing autoimmunity.

This study shows that aging reduces 2,6-linked sialic acids on T cells, leading to exhaustion and impaired immune function.

This study shows that p53 activity, regulated epigenetically, maintains intestinal Treg identity and prevents inflammation by preventing Foxp3 loss in Th17 environments.

The paper shows that ablating tumor-infiltrating Tregs systemically controls tumors without autoimmunity, primarily through CD4+ T cells and cDC2s.

This study shows that TLR2 signaling in innate immune cells within tumors reduces Treg stability, enhancing cancer immunotherapy by improving CD8+ T cell function.

This study shows that increased EZH2 activity in regulatory T cells enhances their effector differentiation and autoimmunity suppression capacity.

The paper develops a mass cytometry method to track T cell receptor repertoires and differentiation states during infection and immunotherapy, showing how antigen recognition influences T cell responses.

This study investigates how different routes of Listeria monocytogenes administration affect tumor growth in mice, finding that IV followed by IT administration controls tumor growth through anti-Lm CD8 T cells.