📣The registration deadline is fast approaching (Feb 3rd) for the upcoming Keystone meeting on Myeloid cells #KSMyeloid26 The line up is looking great and it promises to be a fantastic meeting, so don’t hesitate, if you have not already registered, do it today!
Posts by Charlotte Scott
The Abstract deadline (for short talks) is rapidly approaching for the upcoming Keystone meeting on Myeloid cells to be held at Keystone, CO from 23rd-26th Feb 2026. Have a cool story to share? Submit an abstract before 29th October! More details here: www.keystonesymposia.org/conferences/...
Excited for a full day of science at the IRC Science day today. Such a nice opportunity to learn what everyone is up to at the centre and network in a beautiful venue! @viblifesciences.bsky.social
📢 We are hiring…. Looking for a lab technician to join the team to support our efforts investigating myeloid cell functional heterogeneity in health and disease! Interested? Please apply here: jobso.id/mvfh
My favourite part of being a PI… watching your team members grow and shine! Great talk by @federicodeponti.bsky.social at #EPW2025 super talented PhD student about to defend and looking for a postdoc…. One to watch for the future!
Looking forward to 3 days of fascinating phagocyte biology at #EPW2025 in Madrid kicking off with a great talk from Elvira Mass @masslab.bsky.social
Thank you!
And have just seen that Federico @federicodeponti.bsky.social has made the switch too!
Still a lot of questions to answer of course including what is the fate of these cells after repair, what is the critical mass of LAM-like cells for repair and does timing matter? Looking forward to addressing these next!
This work was not possible without the help from our many collaborators (most of whom still need to switch to Bluesky) for which we are very grateful 🙌
Moreover we demonstrate that LAMs and LAM-like KCs are functionally redundant, whereby TREM2 expression is only required on one of these populations for efficient repair. Loss of TREM2 from both macrophage subsets leads however to impaired repair and exacerbated fibrosis.
Here we show that the LAM phenotype (including TREM2, GPNMB, CD36, CD9) previously shown in recruited macrophages is an activation state that can also be induced on resident KCs in various models of liver injury.