Literature DB >> 1185242

Do neurological signs occur in experimental allergic encephalomyelitis in the absence of inflammatory lesions of the central nervous system?.

S Levine, R Sowinski, C M Shaw, E C Alvord.   

Abstract

Guinea pigs with paralysis or other severe neurological signs of experimental allergic encephalomyelitis (EAE) always exhibited typical histological inflammatory lesions. A few animals inoculated with either the encephalitogenic emulsion or only the control adjuvant emulsion had mild weakness or slowness but no histologic lesion. In some instances, these signs were explained by coincidental non-neural disease or trauma. Therefore, such mild clinical signs cannot be considered pathognominic of EAE. Reports from the literature suggesting that animals have developed clinical signs without histological lesions in EAE are considered invalid because of the nonspecificity of clinical signs, the occurrence of intercurrent diseases, the inadequacy or incorrect timing of histologic evaluations, and the lack of controls for specificity of the signs. There is no basis for the supposition that autoimmunity can cause major neurological signs in the absence of inflammatory lesions in the nervous system.

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Year:  1975        PMID: 1185242     DOI: 10.1097/00005072-197511000-00004

Source DB:  PubMed          Journal:  J Neuropathol Exp Neurol        ISSN: 0022-3069            Impact factor:   3.685


  7 in total

1.  MP4- and MOG:35-55-induced EAE in C57BL/6 mice differentially targets brain, spinal cord and cerebellum.

Authors:  Stefanie Kuerten; Dilyana A Kostova-Bales; Lukas P Frenzel; Justine T Tigno; Magdalena Tary-Lehmann; Doychin N Angelov; Paul V Lehmann
Journal:  J Neuroimmunol       Date:  2007-07-25       Impact factor: 3.478

2.  Chronic relapsing EAE. Time course of neurological symptoms and pathology.

Authors:  H Lassmann; H M Wisniewski
Journal:  Acta Neuropathol       Date:  1978-08-07       Impact factor: 17.088

3.  Experimental allergic encephalomyelitis. Inhibition of clinical signs and paradoxical enhancement of lesions in second attacks.

Authors:  S Levine; R Sowinski
Journal:  Am J Pathol       Date:  1980-11       Impact factor: 4.307

4.  Acute experimental allergic encephalomyelitis in radiation bone marrow chimeras between high and low susceptible strains of mice.

Authors:  R Korngold; A Feldman; L B Rorke; F D Lublin; P C Doherty
Journal:  Immunogenetics       Date:  1986       Impact factor: 2.846

5.  Schwann cell remyelination and recurrent demyelination in the central nervous system of mice infected with attenuated Theiler's virus.

Authors:  M C Dal Canto; H L Lipton
Journal:  Am J Pathol       Date:  1980-01       Impact factor: 4.307

6.  Fundamental differences in the dynamics of CNS lesion development and composition in MP4- and MOG peptide 35-55-induced experimental autoimmune encephalomyelitis.

Authors:  Stefanie Kuerten; Sita Javeri; Magdalena Tary-Lehmann; Paul V Lehmann; Doychin N Angelov
Journal:  Clin Immunol       Date:  2008-08-23       Impact factor: 3.969

7.  Genetic control of resistance to clinical EAE accompanied by histological symptoms.

Authors:  D L Gasser; A Goldner-Sauvé; W F Hickey
Journal:  Immunogenetics       Date:  1990       Impact factor: 2.846

  7 in total

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