The remedy may lie in ourselves: prospects for immune cell therapy in central nervous system protection and repair.

The irreversible loss of function after axonal injury in the central nervous system (CNS) is a result of the lack of neurogenesis, poor regeneration, and the spread of damage caused by toxicity emanating from the degenerating axons to uninjured neurons in the vicinity. Now, 100 years after Ramon y Cajal's discovery that CNS neurons--unlike neurons of the peripheral nervous system--fail to regenerate, it has become evident that (a) CNS tissue is indeed capable of regenerating, at.least in part, provided that it acquires the appropriate conditions for growth support, and (b) that the spread of damage can be stopped and the postinjury rescue of neurons thus achieved, if ways are found to neutralize the mediators of toxicity, either by inhibiting their action or by increasing tissue resistance to them.

Potential repair of rat spinal cord injuries using stimulated homologous macrophages.

The failure of the adult mammalian central nervous system (CNS) to regenerate after injury has long been viewed as a unique phenomenon resulting from the specific nature of this system. The finding that some CNS axons could be induced to regrow if provided with a permissive environment suggested that this failure is a result, at least in part, of the nature of the postinjury neuronal environment. It was further shown that the involvement of inflammatory cells, particularly macrophages, in postinjury processes in the CNS is limited.

Link between optic nerve regrowth failure and macrophage stimulation in mammals.

The adult mammalian central nervous system (CNS) fails to regenerate its axons following injury. A comparison between its postinjury response and that of axons of nervous systems capable of regeneration reveals major differences with respect to inflammation. In regenerative systems, a large number of macrophages rapidly invade the injured site during the first few hours and days after the injury.

Peripheral nerve-stimulated macrophages simulate a peripheral nerve-like regenerative response in rat transected optic nerve.

We have previously demonstrated that the failure of the mammalian central nervous system (CNS) to regenerate following axonal injury is related to its immunosuppressive nature, which restricts the ability of both recruited blood-borne monocytes and CNS-resident microglia to support a process of repair. In this study we show that transected optic nerve transplanted with macrophages stimulated by spontaneously regenerating nerve tissue, e.g.

Restricted inflammatory reaction in the CNS: a key impediment to axonal regeneration?

Axons in the central nervous system (CNS) of adult mammals do not regenerate after injury. Mammalian CNS differs in this respect from other mammalian tissues, including the peripheral nervous system (PNS), and from the CNS of lower vertebrates. In most parts of the body, including the nervous system, injury triggers an inflammatory reaction involving macrophages.