Judit Svensson ArvelundDec 21, 2022

Cool paper dissecting the mechanism of action of #immunecheckpointblockade, anti-CTLA-4, and showing the important role of #myeloidcells #macrophages

"Anti-CTLA-4 antibodies drive myeloid activation and reprogram the tumor microenvironment through FcγR engagement and type I interferon signaling"

#naturecancer #immunotherapy #immunecheckpointinhibitor #macrophages #IFNI

https://www.nature.com/articles/s43018-022-00447-1

Anti-CTLA-4 antibodies drive myeloid activation and reprogram the tumor microenvironment through FcγR engagement and type I interferon signaling - Nature Cancer

Yofe et al. demonstrate that FcγR engagement early after anti-CTLA-4 blockade induces a rapid remodeling of innate immunity and activation of type I interferon signaling, which are crucial for successful anti-CTLA-4 therapy.

Nature
Alex SilverNov 17, 2022
Here's a terrific new paper from one of my classmates about #ImmuneCheckpointInhibitor induced #myocarditis. This work finds that CD8+ T-cells are the critical mediator of heart inflammation, and identifies the alpha-myosin cardiac protein as a candidate autoantigen: https://www.nature.com/articles/s41586-022-05432-3 #science #medicine #immunology #cardiology #oncology #Tcell #genomics #scRNAseq
T cells specific for α-myosin drive immunotherapy-related myocarditis - Nature

Cytotoxic CD8+ T cells specific for α-myosin are identified as pivotal players in myocarditis associated with immune checkpoint inhibitor anticancer therapies.

Nature