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  4. The role of the immune system in central nervous system plasticity after acute injury

The role of the immune system in central nervous system plasticity after acute injury

Neuroscience, 2014 · DOI: 10.1016/j.neuroscience.2014.04.036 · Published: December 26, 2014

ImmunologyNeurology

Simple Explanation

Acute brain injuries trigger rapid cell death, which in turn activates communication between the injured brain and the immune system. In the acute phase, the damaged CNS activates resident and circulating immune cells via the release of soluble mediators, which is necessary to confine the injured tissue and clear cellular debris. The challenge for treating acute CNS damages is to understand how to optimally engage and modify these immune responses, thus providing new strategies that will compensate for tissue lost to injury.

Study Duration
Not specified
Participants
Not specified
Evidence Level
Review article

Key Findings

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    Early immune activation after acute CNS injury might have neuroprotective effects.
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    Sustained inflammation profoundly shapes functional and structural plasticity within the CNS
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    Modulation of the innate or adaptive immune responses represents a promising approach to treat acute CNS disorders.

Research Summary

Acute brain injuries cause rapid cell death that activates bidirectional crosstalks between the injured brain and the immune system. Here we have reviewed the available information about the role and function of the innate and adaptive immune responses in influencing CNS plasticity during the acute and chronic phases of recovery after injury. Future therapies for CNS disorders must be then conceived to execute a fine immune-modulatory tuning in response to the diverse signals of the inflammatory microenvironment.

Practical Implications

Therapeutic Strategies

Modulating immune responses could be a key strategy for treating acute CNS injuries.

Protective Autoimmunity

Enhancing early immune activation may foster CNS repair after injury.

Target Identification

Identifying how sustained immune activation interferes with CNS regeneration can provide valuable therapeutic targets.

Study Limitations

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