David Sancho

🤔Do you think that OXPHOS in DCs = tolerance? 🚨In our new @Cell_Metabolism study @CNIC_CARDIO , we show that active #mitochondrial ETC primes cDC1s for immunogenicity, boosting anti-tumor immunity. Life (and #immunometabolism) is not simple ⚡️(1/9) OPEN: cell.com/cell-metabolis…

@Lo_Zanzi @harvardmed @Harvard Congrats, Ivan! Very deserved!👏🏻👏🏻👏🏻 Lovely dedication to your people! 😍

More than thrilled to share that I’ve been promoted to full (tenured) Professor @harvardmed @Harvard. This only happened because of the hard work of many people, but I want to dedicate this promotion to my grandmas, Nonna Maria & Nonna Vevè. A #FirstGen thread 🧵 1/x

*Postdoc opportunities* Interested in how #dendritic cells or #neutrophils adapt their #metabolism to different tissues in health, #Obesity and #Aging? We are looking for two #Postdoctoral fellows to strengthen our team @IRBBarcelona! Apply at recruitment.irbbarcelona.org/jobs/7609780-p…

5/5 Take-home message: SHP-1 has opposite roles depending on the cell type 👉 Cell-specific targeting could be key for future immunotherapies. Thanks to @ElenaHerndezGa1, Miguel Galán, and Pablo Munné for leading this project.

4/5 cDC1s and macrophages both require SHP-1 to support effective CD8+ T cell responses. Without it: ❌ Fewer CD8+ T cells in tumors ❌ Reduced IFN-γ and cytotoxic function

3/5 Mechanistically, SHP-1 loss dampens IFN-γ signaling and modulates antigen presentation genes in myeloid cells, including ↓ MHC-II in tumor-associated macrophages

2/5 Surprisingly, deleting SHP-1 in CD11c+ cells (mainly dendritic cells and macrophages) worsens tumor control across several tumor models, even with anti–PD-1 therapy.

🧵1/5 New paper together with @SanchoLab🥳: SHP-1 is a widely expressed inhibitory protein tyrosine phosphatase. It can be considered an immune checkpoint target—but its role may depend on the cell type within the tumor microenvironment. frontiersin.org/journals/immun…

@YbpCph @Cell_Metabolism @CNIC_CARDIO @NachoHM3 @SWculek @AgEInves @CienciaGob @ERC_Research @ComunidadMadrid @contracancerINV @criscancer @WorldwideCancer @ContraCancerEs Gracias, Yvelise! 🫂

@SanchoLab @Cell_Metabolism @CNIC_CARDIO @NachoHM3 @SWculek @AgEInves @CienciaGob @ERC_Research @ComunidadMadrid @contracancerINV @criscancer @WorldwideCancer @ContraCancerEs Enhorabuena!

🤔Do you think that OXPHOS in DCs = tolerance? 🚨In our new @Cell_Metabolism study @CNIC_CARDIO , we show that active #mitochondrial ETC primes cDC1s for immunogenicity, boosting anti-tumor immunity. Life (and #immunometabolism) is not simple ⚡️(1/9) OPEN: cell.com/cell-metabolis…

@RyanLab_TCD @Cell_Metabolism @CNIC_CARDIO @NachoHM3 @SWculek @AgEInves @CienciaGob @ERC_Research @ComunidadMadrid @contracancerINV @criscancer @WorldwideCancer @ContraCancerEs Thanks, Dylan! 🫂

@SanchoLab @Cell_Metabolism @CNIC_CARDIO @NachoHM3 @SWculek @AgEInves @CienciaGob @ERC_Research @ComunidadMadrid @contracancerINV @criscancer @WorldwideCancer @ContraCancerEs Great to see this published @SanchoLab, @SWculek & @NachoHM3 👏👏

@eballestar Thanks to you & Pep for a wonderful collaboration & the future collaborations to come! 🫂🫂🫂

Wonderful work, David! The concept that ETC flux—not ATP—licenses cDC1 immunogenicity through /metabolite control of DNA methylation is conceptually beautiful. Congrats to Ignacio, Stefanie and the whole team! Thanks for giving us the chance to learn throught this collaboration!

Led by @NachoHM3 @CNIC_CARDIO & @SWculek @IRBBarcelona Thx to @eballestar & other collaborators & funders: @AgEInves @ministeriodeciencia @ERC_Research @ComunidadMadrid @contracancerINV @ContraCancerEs @WorldwideCancer @criscancer Open access 👉 cell.com/cell-metabolis…

📌 Take‑home: An active #mitochondrial ETC keeps cDC1s poised for rapid #immunogenic responses by tuning redox & #metabolite balance controlling DNA #methylation—independently of ATP.