Immune–tracheal intercellular signalling coordinates the muscle injury response in Drosophila

Effective tissue adaptation to damage requires precise coordination among diverse cell types. In skeletal muscle, the cellular and molecular mechanisms that orchestrate this coordination remain incompletely understood. Here, we identify adult Drosophila immune cells, hemocytes, as central organizers of post-injury muscle repair. Muscle damage triggers rapid recruitment of hemocytes to affected fibers. Hemocyte-derived FGF-like ligand Branchless (Bnl) activates FGF/FGFR signalling on vascular-like tracheal cells, guiding their localized expansion toward injured regions. In parallel, hemocytes deposit extracellular matrix (ECM) components, including Collagen IV, which accumulate around damaged fibers to confine Bnl distribution and facilitate tracheal recruitment. Disruption of hemocyte-mediated Bnl or ECM delivery impairs tracheal remodelling and compromises muscle recovery after injury. Together, these findings reveal an immune–muscle–vascular communication module that integrates signalling and matrix remodelling to preserve muscle function following acute damage.