After injury and regeneration, proteins in newly-formed myelin contribute to resolution of the inflammatory response by facilitating macrophage exit from the basal lamina. A single axon (turquoise) with myelin (green) and basal lamina (purple) is shown in cross-section. 1. In the uninjured peripheral nerve, the myelinated axon is surrounded by many tight wraps of myelin; this unit is covered by the basal lamina. Resident macrophages (pink) perform a surveillance role and are present outside of the basal lamina. 2. After peripheral nerve injury, the axon degenerates and myelin break down begins. Activated resident and hematogenous macrophages accumulate and penetrate the basal lamina, where they phagocytose myelin and axon debris. Because the debris can physically prevent regeneration and also contains inhibitors to axon growth, this macrophage-mediated phagocytosis is a crucial step in nerve repair. 3. After debris phagocytosis, axon regeneration, and remyelination, macrophages are no longer useful within the basal lamina. Proteins on the surface of newly-formed myelin signal debris-laden macrophages to emigrate from the basal lamina. Inset (fourth panel): myelin-associated glycoprotein (MAG), present on myelin membranes, interacts with the receptor NgR and its signaling partner TROY on macrophage membranes. Engagement of this receptor complex in the trailing edge of macrophages leads to local activation of the small GTPase RhoA, which signals for local repulsion and movement away from the source of activation (myelin). Ultimately, this causes macrophage exit from the basal lamina once remyelination has occurred.