As a final note, this whole process is highly relevant not only for killing pathogens, but also in autoimmune diseases.

We could also show that sputum of cystic fibrosis patients contains high levels of MPO functionalised NET-like structures.

This meeting looks fantastic 🤩

All very strong but I love NoBS… might have to edit previous post…

9/n I’m excited to continue to research the interplay between haematopoiesis, inflammation and cancer progression and how we can therapeutically target chronic inflammation in my new lab @mcgillgci.bsky.social

8/n Huge thanks to amazing collaborators @dewitlab.bsky.social for amazing collaboration and to the KWF for funding

7/n Huge thank you to Bluesky-less Karin de Visser for being the best postdoc mentor possible and all her support through the years including 2 mat leaves and covid!

6/n leading to a reversal of neutrophil immunosuppressive phenotype and reduced metastatic spread

5/n Can this tumour-driven education be reversed? Yes! We found treatment with clinically relevant anti-IL-1b normalized tumour-induced granulopoiesis at cellular, transcriptomic and chromatin levels

4/n really intriguingly, we find that tumour-driven immunosuppressive imprinting of neutrophils starts early in haematopoiesis and we can identify genes associated with immunosuppression upregulated in haematopoietic stem cells

3/n Using single-cell, chromatin and functional analyses we unravel tumour-driven reprogramming of granulopoiesis in the bone marrow and find that mammary tumours accelerate commitment to the neutrophil lineage at the expense of lymphocytes and RBCs

2/n We asked how do distant mammary tumours reprogram neutrophil development at the molecular level and when does tumour imprinting occur during neutrophil development

1/n Mammy tumours drive systemic inflammation: in 🚺 and 🐁 we see increased circulating neutrophils that are polarized to an immunosuppressive phenotype which promotes metastatic spread