In the injured adult mammalian central nervous system (CNS), the failure of axonal regeneration is
thought to be attributed, at least in part, to various myelin-associated inhibitors (MAIs), such as Nogo, myelinassociated
glycoprotein (MAG), and oligodendrocyte-myelin glycoprotein (OMgp) around the damaged site. Interestingly,
these three structurally different inhibitors share two common receptors, Nogo-66 receptor (NgR) and
paired immunoglobulin-like receptor B (PirB), and transduce the inhibitory signal into neurons via their complex
combinant and co-receptors, such as p75 neurotrophin receptor (p75NTR), Nogo receptor-interacting protein 1
(LINGO-1), and TROY. Accordingly, targeting of the whole myelin or just portions by immunization has been
proved to be neuroprotective and is able to promote regeneration in the injured spinal cords. In the past few years,
vaccine approaches were initially achieved and could induce the production of antibodies against inhibitors in myelin to block the inhibitory
effects and promote functional recovery in spinal cord injury (SCI) models by immunizing with MAIs, such as purified myelin, spinal
cord homogenates, or their receptors with the concept of protective autoimmunity formulated. However, for safety consideration, further
work is necessary before the immunotherapy strategies can be adopted to treat human injured spinal cords.
Keywords: Immunotherapy, spinal cord injury (SCI), myelin-associated inhibitors (MAIs), Nogo, myelin-associated glycoprotein (MAG),
oligodendrocyte-myelin glycoprotein (OMgp), Nogo-66 receptor (NgR), paired immunoglobulin-like receptor B (PirB), p75 neurotrophin
receptor (p75NTR), Nogo receptor-interacting protein 1 (LINGO-1).
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