Optic neuritis in chronic relapsing experimental allergic encephalomyelitis in Biozzi ABH mice: Demyelination and fast axonal transport changes in disease

O'Neill, J.K.; Baker, David; Morris, Michael; Gschmeissner, Steve; Jenkins, Huw G.; Butt, Arthur M.; Kirvell, Sara; Amor, Sandra

doi:10.1016/s0165-5728(97)00203-8

Cited by 25 publications

(17 citation statements)

References 29 publications

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“…Destruction of oligodendrocytes or myelin leads to disastrous consequences for optic nerve function, and underlies the optic neuritis that is often an early stage of the pathology of the human demyelinating disease, multiple sclerosis (MS). [14][15][16][17] Studies in animal models of MS have demonstrated that optic nerve oligodendrocytes are markedly affected during demyelination in experimental autoimmune encephalomyelitis (EAE), 14 viral induced demyelination, 15 and following treatment with tumour necrosis factor-a (TNF-a), a cytokine implicated in MS ( Figure 2). 16 Demyelination is marked by the attenuation of and, in extreme cases, complete loss of internodal myelin sheaths in individual oligodendrocytes ( Figure 2g-i).…”

Section: Oligodendrocytes and Axoglial Interactionsmentioning

confidence: 99%

“…16 Demyelination is marked by the attenuation of and, in extreme cases, complete loss of internodal myelin sheaths in individual oligodendrocytes ( Figure 2g-i). This results in focal demyelination and the slowed conduction velocities and conduction block characteristic of EAE and MS. 14,17 Remyelination and recovery of axonal function occur during remission in EAE and MS, 14 and this is a function of newly differentiated cells formed from the adult OPC pool. 18 However, in chronic MS, remyelination fails and axonal function is irreversibly compromised, despite the presence of OPCs within lesions.…”

Section: Oligodendrocytes and Axoglial Interactionsmentioning

confidence: 99%

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Functions of optic nerve glia: axoglial signalling in physiology and pathology

Butt

Pugh

Hubbard

et al. 2004

Eye

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An early concept of glial function envisaged them as passive and unexcitable structural elements, much like the connective tissues of organs in the periphery. It is now known that glia have a widespread range of physiological roles and react to all forms of pathological insult. This paper reviews the major functions of oligodendrocytes and astrocytes, the main types of glia in the optic nerve, and examines novel NG2-glia, otherwise known as oligodendrocyte progenitor cells (OPCs). The major function of oligodendrocytes is to produce the myelin sheaths that insulate CNS axons, but they also have important roles in the establishment of nodes of Ranvier, the sites of action potential propagation, and axonal integrity. Astrocytes have multiple physiological and pathological functions, including potassium homeostasis and metabolism, and reactive astrogliosis in response to CNS insults. The bulk of NG2-glia are postmitotic complex cells, distinct from OPCs, and respond to any insult to the CNS by a rapid and stereotypic injury response. This may be their primary unction, but NG2-glia, or a subpopulation of NG2-expressing adult OPCs, also provide remyelinating oligodendrocytes following demyelination. Oligodendrocytes, astrocytes, and NG2-glia all contact axons at nodes of Ranvier and respond to glutamate, ATP, and potassium released during axonal electrical activity. Glutamate and ATP evoke calcium signalling in optic nerve glia and have dual roles in physiology and pathology, coupling glial functions to axonal activity during normal activity, but enhanced activation induces an injury response, as seen following injury, demyelination, and ischaemia.

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Section: Oligodendrocytes and Axoglial Interactionsmentioning

confidence: 99%

Section: Oligodendrocytes and Axoglial Interactionsmentioning

confidence: 99%

Functions of optic nerve glia: axoglial signalling in physiology and pathology

Butt

Pugh

Hubbard

et al. 2004

Eye

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“…For example, immune responses to MBP or PLP induce lesions located predominantly in the spinal cord whereas immunization with MOG generates mainly optic nerve and spinal cord lesions (34). Optic nerve lesions have been reported in some forms of EAE, but have always been associated with the presence of inflammation and demyelination of the brain and spinal cord (9,12,(35)(36)(37). In the present study we take advantage of EAE, model of lesions located predominantly in the optic nerve, to observe the role of the main four T helper cell subsets Th1, Th2, Th17 and Treg during different stages of disease.…”

Section: Discussionmentioning

confidence: 99%

“…Typical characteristics in young adults are sudden monocular loss of vision accompanied by eye pain and it occurs more frequently in women than in men. ON is often observed in patients with multiple sclerosis (MS) (6,7) and experimental autoimmune encephalomyelitis (EAE) in various animal species, including the mouse (5,(8)(9)(10)(11), rat (12), guinea pig (13), and primates (14,15). Development of ON after induction of EAE suggests an autoimmune origin of the optic nerve inflammation observed in MS.…”

Section: Introductionmentioning

confidence: 99%

Alteration of T helper cell subsets in the optic nerve of experimental autoimmune encephalomyelitis

Tian

Zhang²,

Shi³

et al. 2010

Int J Mol Med

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“…Optic nerve lesions have also been reported in EAE [8][9][10], and may represent an early event in the progression of anti-myelin immune responses [11]. The optic nerve may also express increased levels of MOG relative to the spinal cord, suggesting that the increased amount of antigen may facilitate the early activation of self-reactive T cells.…”

Section: Introductionmentioning

confidence: 99%

An MHC anchor‐substituted analog of myelin oligodendrocyte glycoprotein 35–55 induces IFN‐γ and autoantibodies in the absence of experimental autoimmune encephalomyelitis and optic neuritis

Ford

Evavold

2004

Eur J Immunol

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Previous strategies to ameliorate experimental autoimmune encephalitis (EAE) include the treatment of autoreactive T cells with altered peptide ligands, which contain amino acid substitutions at TCR contact residues. We recently showed that a variant of myelin oligodendrocyte glycoprotein (MOG) 35-55 possessing low affinity for MHC (45D) induced anergy in MOG 35-55-specific T cells and reduced their encephalitogenicity upon adoptive transfer. Here we investigate the characteristics of the primary immune response to this MHC anchorsubstituted peptide. Overall, we observed that immunization with 45D resulted in the production of IFN-+ and anti-MOG 35-55 autoantibodies at levels similar to those of MOG 35-55-immunized mice with active EAE. However, no symptoms of clinical or histological EAE or overt histological optic neuritis were observed in 45D-immunized mice. Consistent with this finding, 45D-immunized mice did not exhibit CD4 + infiltrates into the CNS. Therefore, MOG 35-55-specific precursors stimulated with a weak ligand (45D) mediate some EAE-associated effector functions but are unable to fully initiate the inflammatory process in the central nervous system that leads to clinical manifestation of EAE.

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Optic neuritis in chronic relapsing experimental allergic encephalomyelitis in Biozzi ABH mice: Demyelination and fast axonal transport changes in disease

Cited by 25 publications

References 29 publications

Functions of optic nerve glia: axoglial signalling in physiology and pathology

Functions of optic nerve glia: axoglial signalling in physiology and pathology

Alteration of T helper cell subsets in the optic nerve of experimental autoimmune encephalomyelitis

An MHC anchor‐substituted analog of myelin oligodendrocyte glycoprotein 35–55 induces IFN‐γ and autoantibodies in the absence of experimental autoimmune encephalomyelitis and optic neuritis

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