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In normal optic nerves (ON) constitutive IL\u201018 mRNA levels as revealed by semiquantitative reverse transcriptase polymerase chain reaction were higher than in sciatic nerves (SN). After nerve crush, steady\u2010state levels moderately increased in the distal nerve part of the SN but not the ON. By immunocytochemistry no SN or faint ON IL\u201018 protein expression was detectable in normal nerves. In contrast, IL\u201018 expression dramatically increased after SN and ON crush. On the cellular level, ED1<jats:sup>+<\/jats:sup> macrophages infiltrating the crush site strongly expressed IL\u201018 at days 2 and 4 after SN crush. By days 4 and 8, in addition, the entire distal nerve part was covered by IL\u201018<jats:sup>+<\/jats:sup> macrophages. At day 16, IL\u201018 immunoreactivity had disappeared despite the presistence of large numbers of ED1<jats:sup>+<\/jats:sup> macrophages. A similar infiltration of IL\u201018<jats:sup>+<\/jats:sup> macrophages was seen at the crush site in the ON. Moreover, microglia in the distal ON stump lacking macrophage infiltration and undergoing delayed myelin degradation up\u2010regulated IL\u201018. In conclusion this study shows that IL\u201018 is involved in the cytokine network associated with the robust inflammatory response during WD of the SN. Despite up\u2010regulation of the proinflammatory cytokine IL\u201018, major histocompatiblity complex class II, and CD4 molecules similar to macrophages in the PNS, microglial activation after ON injury appears to be insufficient to mount an effective phagocytic response as a prerequisite for successful regeneration in the CNS. J. Neurosci. 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