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Allergic Encephalomyelitis

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Arthur Saltzman – One of the best experts on this subject based on the ideXlab platform.

  • Accelerated response to reinoculation in experimental Allergic Encephalomyelitis : clinical study
    International archives of allergy and applied immunology, 1991
    Co-Authors: Seymour Levine, Arthur Saltzman
    Abstract:

    An attack of experimental Allergic Encephalomyelitis is generally thought to confer resistance to a second attack. Nevertheless, some authors have produced second attacks, sometimes with an anamnestic shortening of the incubation period. In addition, second attacks of experimental Allergic Encephalomyelitis with accelerated onsets following reinoculation were found in every experiment when histopathologic rather than clinical criteria were employed. In the present work, we found that clinical signs with accelerated onset were also found in each experiment provided that the first attack was produced with the aid of Freund’s complete adjuvant and provided that the reinoculation stimulus was the highly potent combination of rat spinal cord and carbonyl iron. Whatever the potency of the reinoculation, and regardless of the occurrence of an accelerated onset, the eventual outcome was a decreased severity and mortality of the second attack of experimental Allergic Encephalomyelitis. The new data demonstrate that accelerated onset is not necessarily an indication of increased severity.

Joan Goverman – One of the best experts on this subject based on the ideXlab platform.

  • Passive induction of experimental Allergic Encephalomyelitis.
    Nature protocols, 2006
    Co-Authors: Ingunn M. Stromnes, Joan Goverman
    Abstract:

    Experimental Allergic Encephalomyelitis (EAE) is a widely used animal model of the human demyelinating disease multiple sclerosis. EAE is initiated by immunization with myelin antigens in adjuvant or by adoptive transfer of myelin-specific T cells, resulting in inflammatory infiltrates and demyelination in the central nervous system. Induction of EAE in rodents typically results in ascending flaccid paraparalysis with inflammation primarily targeting the spinal cord. This protocol describes passive induction of EAE by adoptive transfer of T cells isolated from mice primed with myelin antigens into naive mice. The advantages of using this method versus active induction of EAE are discussed.

  • active induction of experimental Allergic Encephalomyelitis
    Nature Protocols, 2006
    Co-Authors: Ingunn M. Stromnes, Joan Goverman
    Abstract:

    This protocol details a method to actively induce experimental Allergic Encephalomyelitis (EAE), a widely used animal model for studies of multiple sclerosis. EAE is induced by stimulating T-cell-medimediated immuimmunity to myelin antigens. Active induction of EAE is accomplished by immunization with myelin antigens emulsified in adjuvant. This protocol focuses on induction of EAE in mice; however, the same principles apply to EAE induction in other species. EAE in rodents is manifested typically as ascending flaccid paraparalysis with inflammation targeting the spinal cord. However, more diverse clinical signs can occur in certain strain/antigen combinations in rodents and in other species, reflecting increased inflammation in the brain.

Hong Jiang – One of the best experts on this subject based on the ideXlab platform.

  • Angiopoietin-1 and C16 Peptide Attenuate Vascular and Inflammatory Responses in Experimental Allergic Encephalomyelitis.
    Cns & Neurological Disorders-drug Targets, 2016
    Co-Authors: Beibei Wang, Ke-wei Tian, Fan Zhang, Hong Jiang
    Abstract:

    Breakdown of normal blood-brain barrier function and accompanying vascular leakage are fundamental stages in the onset of multiple sclerosis and its animal counterpart, experimental Allergic Encephalomyelitis. In the present study, angiopoietin-1, an endothelial growth factor well known for its role in establishing and maintaining vascular integrity, and C16, a peptide that competitively binds to integrin αvβ3 expressed on endothelial cells, were used to treat acute experimental Allergic Encephalomyelitis in Lewis rats. Angiopoietin-1 was more effective than C16 for reducing inflammation-induced vascular leakage. Moreover, treatment with a combination of angiopoietin-1 and C16 resulted in greater effects, not only in alleviating inflammation and reducing axonal loss/demyelination but also in down-regulating pro-inflammatory cytokine expression and improving electrophysiological dysfunction, than treatment with either angiopoietin-1 or C16 alone. Different protective effects were observed with angiopoietin-1 and C16 treatment suggesting that these proteins target specific receptors to act through different pathways. Furthermore, angiopoietin-1 and C16 may form the basis of a promising therapeutic strategy for experimental Allergic Encephalomyelitis and multiple sclerosis.

Ellen Heber-katz – One of the best experts on this subject based on the ideXlab platform.

  • T-cell receptor peptide immunization leads to enhanced and chronic experimental Allergic Encephalomyelitis
    Proceedings of the National Academy of Sciences of the United States of America, 1991
    Co-Authors: L Desquenne-clark, T R Esch, Laszlo Otvos, Ellen Heber-katz
    Abstract:

    Abstract It has previously been reported that synthetic peptides corresponding to sequences derived from T-cell receptor variable regions identified as dominant in the T-cell-mediated autoimmune disease experimental Allergic Encephalomyelitis in both the mouse and the rat can down-regulate disease in Lewis rats. In contrast to these results, we have found that immunization of Lewis rats with such peptides in complete Freund‘s adjuvant prior to induction of experimental Allergic Encephalomyelitis with myelin basic protprotein leads to responses ranging from profound disease enhancement to lack of disease. In some cases, enhanced disease was followed by a prolonged neurologic deficit that resembles multiple sclerosis more closely than does acute experimental Allergic Encephalomyelitis. These findings, on the one hand, support previous results showing T-cell receptor peptide-induced modulation of the disease experimental Allergic Encephalomyelitis and, on the other, indicate that such immunization is not a reliable method for inducing suppression of encephalitogenic effector cells.

Seymour Levine – One of the best experts on this subject based on the ideXlab platform.

  • Accelerated response to reinoculation in experimental Allergic Encephalomyelitis : clinical study
    International archives of allergy and applied immunology, 1991
    Co-Authors: Seymour Levine, Arthur Saltzman
    Abstract:

    An attack of experimental Allergic Encephalomyelitis is generally thought to confer resistance to a second attack. Nevertheless, some authors have produced second attacks, sometimes with an anamnestic shortening of the incubation period. In addition, second attacks of experimental Allergic Encephalomyelitis with accelerated onsets following reinoculation were found in every experiment when histopathologic rather than clinical criteria were employed. In the present work, we found that clinical signs with accelerated onset were also found in each experiment provided that the first attack was produced with the aid of Freund’s complete adjuvant and provided that the reinoculation stimulus was the highly potent combination of rat spinal cord and carbonyl iron. Whatever the potency of the reinoculation, and regardless of the occurrence of an accelerated onset, the eventual outcome was a decreased severity and mortality of the second attack of experimental Allergic Encephalomyelitis. The new data demonstrate that accelerated onset is not necessarily an indication of increased severity.