Injury to the central nervous system leads to cellular changes not only in
the affected neurons but also in adjacent glial cells. This neuroglial acti
vation is a consistent feature in almost all forms of brain pathology and a
ppears to reflect an evolutionarily-conserved program which plays an import
ant role for the repair of the injured nervous system. Recent work in mice
that are genetically-deficient for different cytokines (M-CSF, IL-6, TNF-al
pha, TGF-beta 1) has begun to shed light on the molecular signals that regu
late this cellular response. Here, the availability of cytokine-deficient a
nimals with reduced or abolished neuroglial activation provides a direct ap
proach to determine the function of the different components of the cellula
r response leading to repair and regeneration following neural trauma.