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In the central nervous system (CNS), IL\u201010 is mainly produced by astrocytes and microglia and it is upregulated after various insults, such as experimental autoimmune encephalomyelitis, middle cerebral artery occlusion, excitotoxicity and traumatic brain injury. To better understand the effects of IL\u201010 in the normal and injured CNS, we generated transgenic mice (termed GFAP\u2010IL\u201010Tg) that expressed the murine <jats:italic>IL\u201010<\/jats:italic> gene under the transcriptional control of the glial fibrillary acidic protein (GFAP) promoter. Previous studies demonstrated marked changes in the microglial phenotype in these mice under basal conditions. The objective of the present study was to investigate the effects of local astrocyte\u2010targeted IL\u201010 production on glial activation, neuronal degeneration and leukocyte recruitment after axotomy. GFAP\u2010IL\u201010Tg mice had marked changes in the phenotype of activated microglial cells, as well as in the number of microglial clusters and in microglial cell density. These microglial changes are accompanied by a twofold increase in lymphocyte infiltration in GFAP\u2010IL\u201010Tg mice and around twofold decrease in neuronal cell death at 21 dpi. Altogether, our findings suggested that astrocyte\u2010targeted production of IL\u201010 impacted the microglial response and lymphocyte recruitment and culminated in a beneficial effect on neuronal survival. 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