In IL-12.aFOLR2.CAR–treated tumors, cancer cells are closely juxtaposed with GZMB⁺ CD8⁺ T cells, consistent with antigen-dependent cytotoxic engagement. But that's not the only way the cancer cells die! To find out more, see the paper for full data, figures and the amazing co-authors!

This resulted in tumor control in models of disseminated ovarian and lung cancer, even though the CAR T cells were not targeting cancer cells.

At low dose and without prior lymphodepletion, this therapy triggered a profound resetting and reprogramming of the TME, with significant infiltration of endogenous CD8 T cells reactive to tumor cells and immunostimulatory CXCL9+ macrophages.

We describe IL-12–armored CAR T cells that target tumor-associated macrophages rather than cancer cells, by recognizing the tumor macrophage markers FOLR2 or TREM2. We show these CAR T cells both kill immunosuppressive tumor macrophages and localize IL-12 activity within the tumor microenvironment.

With co-authors Bram Teunissen & @yizhoudonglab.bsky.social, we dive into emerging ways to make LNPs more precise—from tuning their chemistry to reprogramming RNA expression and even controlling protein stability & localization >>> a road🗺️ for more intelligent delivery & broader applications ahead.

A major hurdle for next-gen LNPs? We still don’t have great tools to see where they go or what they do in vivo.

Tracking the nanoparticle, RNA cargo, and protein output in real time is key to designing smarter, more targeted systems.