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We began analyzing https://link.springer.com/article/10.1007/s001090050092, but it redirected us to https://link.springer.com/article/10.1007/s001090050092. The analysis below is for the second page.

Title[redir]:
Myelin oligodendrocyte glycoprotein: a novel candidate autoantigen in multiple sclerosis | Journal of Molecular Medicine
Description:
โ€‚Myelin oligodendrocyte glycoprotein (MOG) is a member of the immunoglobulin superfamily expressed exclusively in central nervous system (CNS) myelin. While the function of MOG is unknown, a number of studies have shown that immune responses to MOG contribute to the autoimmune-mediated demyelination seen in animals immunized with whole CNS tissue. This paper summarizes our recent studies, which unequivocally demonstrate that MOG by itself is able to generate both an encephalitogenic T cell response and an autoantibody response in Lewis rats and in several strains of mice. In Lewis rats the injection of both native MOG and MOG35โ€“55 peptide produces a paralytic relapsing-remitting neurological disease with extensive plaque-like demyelination. The antibody response to MOG35โ€“55 was highly restricted, as no reactivity to either other MOG peptides or myelin proteins could be detected. Fine epitope mapping showed that antibody from serum and cerebrospinal fluid of injected rats reacted strongly to MOG37โ€“46, which is contiguous to the dominant T cell epitope contained within MOG44โ€“55. NOD/Lt and C57BL/6 mice were also susceptible to severe neurological disease following injection with recombinant MOG or MOG35โ€“55 peptide, indicating that this specific CNS autoantigen, or some of its determinants, can induce a pathogenic response across animal species. Severe paralysis and extensive demyelination were seen in both strains, but NOD/Lt mice experienced a chronic relapsing disease whereas C57BL/6 mice had a chronic non-remitting disease. Moreover, transfer of MOG35โ€“55 T cells into naive NOD/Lt mice also produced severe neurological impairment as well as histological lesions. These results emphasize that a synergism between a T cell-response and anti-MOG antibodies may be important for the development of severe demyelinating disease. This, together with our demonstration that there is a predominant T cell response to MOG in patients with multiple sclerosis, clearly indicates that MOG is probably an important target autoantigen in this disease.

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Keywords {๐Ÿ”}

mog, article, myelin, disease, access, oligodendrocyte, response, privacy, cookies, content, journal, glycoprotein, autoantigen, multiple, sclerosis, demyelination, mice, information, publish, search, cns, severe, antibodies, autoimmune, open, data, log, research, bernard, johns, slavin, cell, rats, neurological, nodlt, discover, springer, function, optional, personal, parties, policy, find, track, molecular, medicine, candidate, cite, ichikawa, ewing,

Topics {โœ’๏ธ}

human autoimmune encephalomyelitis myelin-reactive antibodies initiate myelin oligodendrocyte glycoprotein autoimmune-mediated demyelination month download article/chapter nod/lt mice experienced naive nod/lt mice multiple sclerosis molecular medicine aims related subjects privacy choices/manage cookies full article pdf anti-mog antibodies specific cns autoantigen severe neurological disease important target autoantigen check access instant access cell epitope contained chronic relapsing disease severe demyelinating disease european economic area scope submit manuscript central nervous system la trobe university conditions privacy policy accepting optional cookies extensive demyelination journal finder publish article journal mog35โ€“55 peptide produces myelin proteins pathogenic immune response article log candidate autoantigen nod/lt remitting disease article cite article bernard demyelination privacy policy personal data books a myelin optional cookies manage preferences severe paralysis cell response cell-response journal publish

Schema {๐Ÿ—บ๏ธ}

WebPage:
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         headline:Myelin oligodendrocyte glycoprotein: a novel candidate autoantigen in multiple sclerosis
         description:โ€‚Myelin oligodendrocyte glycoprotein (MOG) is a member of the immunoglobulin superfamily expressed exclusively in central nervous system (CNS) myelin. While the function of MOG is unknown, a number of studies have shown that immune responses to MOG contribute to the autoimmune-mediated demyelination seen in animals immunized with whole CNS tissue. This paper summarizes our recent studies, which unequivocally demonstrate that MOG by itself is able to generate both an encephalitogenic T cell response and an autoantibody response in Lewis rats and in several strains of mice. In Lewis rats the injection of both native MOG and MOG35โ€“55 peptide produces a paralytic relapsing-remitting neurological disease with extensive plaque-like demyelination. The antibody response to MOG35โ€“55 was highly restricted, as no reactivity to either other MOG peptides or myelin proteins could be detected. Fine epitope mapping showed that antibody from serum and cerebrospinal fluid of injected rats reacted strongly to MOG37โ€“46, which is contiguous to the dominant T cell epitope contained within MOG44โ€“55. NOD/Lt and C57BL/6 mice were also susceptible to severe neurological disease following injection with recombinant MOG or MOG35โ€“55 peptide, indicating that this specific CNS autoantigen, or some of its determinants, can induce a pathogenic response across animal species. Severe paralysis and extensive demyelination were seen in both strains, but NOD/Lt mice experienced a chronic relapsing disease whereas C57BL/6 mice had a chronic non-remitting disease. Moreover, transfer of MOG35โ€“55 T cells into naive NOD/Lt mice also produced severe neurological impairment as well as histological lesions. These results emphasize that a synergism between a T cell-response and anti-MOG antibodies may be important for the development of severe demyelinating disease. This, together with our demonstration that there is a predominant T cell response to MOG in patients with multiple sclerosis, clearly indicates that MOG is probably an important target autoantigen in this disease.
         datePublished:
         dateModified:
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            Key wordsโ€‚Myelin oligodendrocyte glycoprotein
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            Experimental autoimmune encephalomyelitis
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      headline:Myelin oligodendrocyte glycoprotein: a novel candidate autoantigen in multiple sclerosis
      description:โ€‚Myelin oligodendrocyte glycoprotein (MOG) is a member of the immunoglobulin superfamily expressed exclusively in central nervous system (CNS) myelin. While the function of MOG is unknown, a number of studies have shown that immune responses to MOG contribute to the autoimmune-mediated demyelination seen in animals immunized with whole CNS tissue. This paper summarizes our recent studies, which unequivocally demonstrate that MOG by itself is able to generate both an encephalitogenic T cell response and an autoantibody response in Lewis rats and in several strains of mice. In Lewis rats the injection of both native MOG and MOG35โ€“55 peptide produces a paralytic relapsing-remitting neurological disease with extensive plaque-like demyelination. The antibody response to MOG35โ€“55 was highly restricted, as no reactivity to either other MOG peptides or myelin proteins could be detected. Fine epitope mapping showed that antibody from serum and cerebrospinal fluid of injected rats reacted strongly to MOG37โ€“46, which is contiguous to the dominant T cell epitope contained within MOG44โ€“55. NOD/Lt and C57BL/6 mice were also susceptible to severe neurological disease following injection with recombinant MOG or MOG35โ€“55 peptide, indicating that this specific CNS autoantigen, or some of its determinants, can induce a pathogenic response across animal species. Severe paralysis and extensive demyelination were seen in both strains, but NOD/Lt mice experienced a chronic relapsing disease whereas C57BL/6 mice had a chronic non-remitting disease. Moreover, transfer of MOG35โ€“55 T cells into naive NOD/Lt mice also produced severe neurological impairment as well as histological lesions. These results emphasize that a synergism between a T cell-response and anti-MOG antibodies may be important for the development of severe demyelinating disease. This, together with our demonstration that there is a predominant T cell response to MOG in patients with multiple sclerosis, clearly indicates that MOG is probably an important target autoantigen in this disease.
      datePublished:
      dateModified:
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      pageEnd:88
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         Multiple sclerosis
         Experimental autoimmune encephalomyelitis
         Demyelination
         Autoantigen
         Molecular Medicine
         Human Genetics
         Internal Medicine
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