Myelin sheath surrounding axons ensures neuronal support and increases conduction speed. Demyelination can occur in many circumstances leading to neurological deficits. Spontaneous remyelination exists but is highly variable among patients and structures. Parenchymal oligodendrocyte progenitor cells (pOPC) are known to contribute to remyelination but the role of neural stem/progenitor cells located in the subventricular zone (SVZdNP) is still debated. In this work, we investigated in a mouse model of demyelination, the contribution of these 2 cell populations in myelin repair. Using genetic cell tracing, we demonstrated that pOPC and SVZdNP contribute equally to corpus callosum (CC) remyelination but in a regionalized manner. CC areas with high SVZdNP mobilization are those less affected by cuprizone. We observed that some SVZdNP mobilized in the demyelinated CC remain undifferentiated and postulated that these progenitors may protect from demyelination via immunomodulation. Using single cell RNA sequencing, we showed that microglia located in CC areas enriched in SVZdNP exhibited a less inflammatory profile than microglia located in areas with high pOPC mobilization. Moreover, we identified a candidate factor in the dialog between SVZdNP and microglia: MFGE8 (milk fat globule-epidermal growth factor-8). MFGE8 is significantly enriched in immature SVZdNP and is implicated in phagocytosis pathway. We showed that MFGE8 treatment or conditioned media from SVZdNP cultures increase myelin debris phagocytosis by microglial cells in culture. Myelin debris clearance is a key step in myelin regeneration. This work highlights the dual role of SVZdNP in myelin regeneration.