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.