Identification of the neuritogen for experimental allergic neuritis

Kadlubowski, M.; Hughes, Richard A.

doi:10.1038/277140a0

Cited by 187 publications

(70 citation statements)

References 15 publications

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“…In common with many myelin proteins, injection of purified P2 protein (Kadlubowski & Hughes, 1979) or neuritogenic peptides derived from it (Uyemura et al, 1982) into experimental animals results in an experimental allergic neuritis (EAN). In the case of P2, an animal model for Guillain-Barré syndrome, a demyelinating disease of human PNS, is produced.…”

Section: Introductionmentioning

confidence: 99%

Structure of myelin P2 protein from equine spinal cord

et al. 2005

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Equine P2 protein has been isolated from horse spinal cord and its structure determined to 2.1 Å . Since equine myelin is a viable alternative to bovine tissue for large-scale preparations, characterization of the proteins from equine spinal cord myelin has been initiated. There is an unusually high amount of P2 protein in equine CNS myelin compared with other species. The structure was determined by molecular replacement and subsequently refined to an R value of 0.187 (R free = 0.233). The structure contains a molecule of the detergent LDAO and HEPES buffer in the binding cavity and is otherwise analogous to other cellular retinol-binding proteins.

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Section: Introductionmentioning

confidence: 99%

Structure of myelin P2 protein from equine spinal cord

et al. 2005

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“…P2 protein, one of the major proteins found in peripheral nervous system (PNS) myelin, has been identified as an antigen responsible for induction of experimental autoimmune neuritis (EAN) (1)(2)(3). EAN is an inflammatory demyelinating disease of the PNS and is considered to be an appropriate model for a human demyelinating disease, the Guillain-Barre syndrome.…”

Section: Introductionmentioning

confidence: 99%

“…The disease-inducing activity of P2 protein alone is much milder than that of whole myelin (1)(2)(3)8). Lipids such as phosphatidylserine (PS) (9,10) The antigenic determinant of bovine P2 protein has been located within the region defined by residues 53-78 (14,15).…”

Section: Introductionmentioning

confidence: 99%

Effect of lipids on the conformation of an antigenic determinant for experimental autoimmune neuritis

Shin¹

1998

IUBMB Life

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SUMMARYThe conformation of SP-26, the synthetic peptide (residues 53-78) of myelin P2 protein that causes experimental autoimmune neuritis (EAN) in the peripheral nervous system, has been studied in lipid environments and in water/trifluoroethanol (TFE) mixture using circular dichroism (CD) spectroscopy and Fourier transform infra-red (FTIR) spectroscopy. SP-26 becomes more structured on binding with micelles formed from anionic lipids and in the presence of TFE. On the other hand, zwitterionic lipids have a denaturing effect or no effect on the conformation of SP-26. The present results suggest that the disease-modulating effects of various lipids are closely related to their ability to induce conformational change in the antigenic region of P2 protein.

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“…Experimental allergic neuritis (EAN) is an autoimmune demyelinating disease of the peripheral nervous system (PNS) induced by inoculation with PNS tissue [1] or P2 protein [2] and adjuvants. In its acute form, it is widely studied as an animal model of the human disorder, the Guillain-Barré syndrome.…”

Section: Introductionmentioning

confidence: 99%

“…These electrophysiological findings correlated well with the histological findings of inflammation and prominent demyelination in the dorsal root ganglia and dorsal roots with minimal involvement of the proximal spinal nerve and no involvement of the sciatic nerve. It is concluded that the hindlimb ataxia in rats with this form of acute experimental allergic neuritis is due to demyelination-induced nerve conduction block in the dorsal root ganglia and probably in the dorsal roots.Experimental allergic neuritis (EAN) is an autoimmune demyelinating disease of the peripheral nervous system (PNS) induced by inoculation with PNS tissue [1] or P2 protein [2] and adjuvants. In its acute form, it is widely studied as an animal model of the human disorder, the Guillain-Barré syndrome.…”

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confidence: 99%

Focal conduction block in the dorsal root ganglion in experimental allergic neuritis

Stanley¹,

McCombe²,

Pender³

1992

Annals of Neurology

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Acute experimental allergic neuritis was induced in Lewis rats by inoculation with bovine intradural root myelin and adjuvants. In terminal experiments, sensory conduction was assessed in rats with hindlimb ataxia and weakness by stimulating the exposed sciatic nerve and recording directly from the exposed L-4 spinal nerve, dorsal root ganglion, dorsal root, and dorsal root entry zone. Focal conduction block was present in a high proportion of large-diameter fibers in the dorsal root ganglion. In contrast, nerve conduction in the peripheral nerve and spinal nerve was essentially normal apart from probable conduction block in some fibers in the proximal spinal nerve in a minority of rats. The afferent volley arriving at the dorsal root entry zone of the spinal cord was greatly reduced, as a consequence of the conduction block in the dorsal root ganglion and probable conduction block in the dorsal root. The M wave recorded from the fourth dorsal interosseus muscle of the hindfoot was normal in amplitude but slightly prolonged in latency and the H reflex was absent. These electrophysiological findings correlated well with the histological findings of inflammation and prominent demyelination in the dorsal root ganglia and dorsal roots with minimal involvement of the proximal spinal nerve and no involvement of the sciatic nerve. It is concluded that the hindlimb ataxia in rats with this form of acute experimental allergic neuritis is due to demyelination-induced nerve conduction block in the dorsal root ganglia and probably in the dorsal roots.Experimental allergic neuritis (EAN) is an autoimmune demyelinating disease of the peripheral nervous system (PNS) induced by inoculation with PNS tissue [1] or P2 protein [2] and adjuvants. In its acute form, it is widely studied as an animal model of the human disorder, the Guillain-Barré syndrome. The distribution of lesions in the PNS differs among different models of acute EAN. In rabbits and mice with acute EAN induced by inoculation with whole PNS tissue, the dorsal root ganglion is the most consistently affected region of the PNS [1,3]. The dorsal root ganglion is also a major site of involvement in rats with PNS myelin-induced or P2-induced acute EAN [4,5]. Electrophysiological studies in animals with acute EAN have demonstrated conduction abnormalities in the PNS [6-14], but have not assessed whether focal conduction block occurs in the dorsal root ganglion. We have previously demonstrated focal conduction block in the dorsal root ganglia of rabbits and, to a lesser extent, in rats with acute experimental allergic encephalomyelitis, an autoimmune demyelinating disease that affects the central nervous system and also results in PNS lesions similar to those of EAN [ 1 5 -1 8 ] . The present study was undertaken to determine whether similar focal conduction block occurs in the dorsal root ganglion in rats with EAN. Materials and Methods Induction of EANFemale Lewis rats (JC strain) bred by the Central Animal Breeding House of the University of Queensland (Brisban...

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Identification of the neuritogen for experimental allergic neuritis

Cited by 187 publications

References 15 publications

Structure of myelin P2 protein from equine spinal cord

Structure of myelin P2 protein from equine spinal cord

Effect of lipids on the conformation of an antigenic determinant for experimental autoimmune neuritis

Focal conduction block in the dorsal root ganglion in experimental allergic neuritis

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