After spinal cord injury (SCI), immune cells and glia are corralled to create a protective barrier around the lesion to prevent the spread of tissue injury and promote wound healing. A new study published in Nature Neuroscience has shown that this process depends on upregulation of the transmembrane receptor Plexin B2 in injury-activated microglia and macrophages (IAMs). The researchers found that in mice, Plexin B2 was induced in IAMs early after SCI and facilitated the formation of concentric rings of microglia and astrocytes around the necrotic core of the lesion. Ablation of Plexin B2 in myeloid cells impaired wound healing and motor–sensory recovery in a mouse model of SCI, further underlining the importance of this receptor for CNS repair.