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Confounding influence

Nature Reviews Neuroscience volume 9, pages 802–803 (2008)Cite this article

A study carried out in Steve Lacroix's laboratory suggests that CD11b+ myeloid cells (a class that includes granulocytes and macrophages) are required for axon regeneration in the PNS. Using mice in which CD11b+ cells were selectively depleted using an inducible suicide gene system, they found that the recovery of sciatic nerve function and peripheral nerve axon regeneration were severely compromised after injury. Furthermore, they showed that CD11b+ cell depletion did not affect neuron viability or the expression of regeneration-associated genes in the cell body, suggesting that rather than regulating the neurons' intrinsic regeneration capacity, CD11b+ cells contribute to the creation of a permissive growth environment. They seem to do so by clearing inhibitory myelin debris, promoting the synthesis and release of neurotrophins by surrounding non-neuronal cells, and stimulating the formation and stabilization of blood vessels at the lesion site.

By contrast, experiments carried out in Jerry Silver's laboratory suggest that the physical contact between macrophages and injured axons is detrimental to axon regeneration in the CNS. Following spinal cord injury in rats, this group found that retracting axons were associated with ED-1-expressing macrophages. When these cells were depleted by injecting clodronate-containing liposomes, which specifically induce macrophage apoptosis, a significant reduction in axonal retraction after injury was observed.

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ORIGINAL RESEARCH PAPERS

  1. Barrette, B. et al. Requirement of myeloid cells for axon regeneration. J. Neurosci. 28, 9363–9376 (2008)

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  2. Horn, K. P., Busch, S. A., Hawthorne, A. L., van Rooijen, N. & Silver, J. Another barrier to regeneration in the CNS: activated macrophages induce extensive retraction of dystrophic axons through direct physical interactions. J. Neurosci. 28, 9330–9341 (2008)

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Authors
  1. Monica Hoyos Flight
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Flight, M. Confounding influence. Nat Rev Neurosci 9, 802–803 (2008). https://doi.org/10.1038/nrn2518

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