Literature DB >> 17512611

Characterization of a severe parenchymal phenotype of experimental autoimmune encephalomyelitis in (C57BL6xB10.PL)F1 mice.

Michael D Carrithers1, Lisette M Carrithers, Jan Czyzyk, Octavian Henegariu.   

Abstract

We here describe a novel CD4 T cell adoptive transfer model of severe experimental autoimmune encephalomyelitis in (C57BL6xB10.PL)F1 mice. This FI cross developed severe disease characterized by extensive parenchymal spinal cord and brain periventricular white matter infiltrates. In contrast, B10.PL mice developed mild disease characterized by meningeal predominant infiltrates. As determined by cDNA microarray and quantitative real time PCR expression analysis, histologic and flow cytometry analysis of inflammatory infiltrates, and attenuation of disease in class I-deficient and CD8-depleted F1 mice; this severe disease phenotype appears to be regulated by CNS infiltration of CD8 T lymphocytes early in the disease course.

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Year:  2007        PMID： 17512611      PMCID： PMC2745253          DOI： 10.1016/j.jneuroim.2007.04.007

Source DB:  PubMed          Journal:  J Neuroimmunol        ISSN： 0165-5728            Impact factor:   3.478


  44 in total

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4.  Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination.

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7.  Intrathecal delivery of IFN-gamma protects C57BL/6 mice from chronic-progressive experimental autoimmune encephalomyelitis by increasing apoptosis of central nervous system-infiltrating lymphocytes.

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8.  Failure to suppress the expansion of the activated CD4 T cell population in interferon gamma-deficient mice leads to exacerbation of experimental autoimmune encephalomyelitis.

Authors:  C Q Chu; S Wittmer; D K Dalton
Journal:  J Exp Med       Date:  2000-07-03       Impact factor: 14.307

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Authors:  T Brabb; P von Dassow; N Ordonez; B Schnabel; B Duke; J Goverman
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