SOCS3 Attenuates GM-CSF/IFN-c-Mediated Inflammation During Spontaneous Spinal Cord Regeneration

Traumatic spinal cord injury (SCI) always results in an excessive inflammatory response, which contributes to secondary tissue damage. SOCS3, a feedback inhibitor of the JAK/STAT signal pathway, negatively regulates axonal regrowth and inflammation in the central nervous system (CNS). Unlike mammals, regenerating organisms such as fish, amphibians, and reptiles are capable of spinal cord regeneration after injury.

• 1
  Severing the gecko spinal cord did not evoke an inflammatory cascade except for an injury-stimulated elevation of the granulocyte/macrophage colony-stimulating factor (GM-CSF) and interferon gamma (IFN-c) cytokines.
• 2
  Enforced expression of SOCS3 was sufficient to suppress the GM-CSF/IFN-c-driven inflammatory responses through its KIR domain by attenuating the activities of JAK1 and JAK2.
• 3
  SOCS3 is specifically induced in the microglia rather than in the neurons of the regenerating spinal cord.