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Friend to the brain, foe to the spine

View Article: PubMed Central

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Regional responses to interferon-γ (IFNγ) dictated whether the spinal cord or cerebellum came under fire in mice with EAE, a mouse model of human multiple sclerosis (MS)... In classical EAE, the T cell attack is focused on the spinal cord... But in atypical disease, the cerebellum and brain stem are the primary victims... A prior study suggested that the ratio of interleukin (IL)-17 to IFNγ determines whether disease pathology occurs in the spine or brain, with increasing levels of IL-17 associated with disease in the brain... But when transferred into mice lacking the IFNγ receptor, the cells instead attacked the cerebellum and brain stem, sparing the spinal cord... The production of IL-17 by the transferred T cells was comparable in both settings... However, the production of IL-17 by non-T cells predominated in the cerebellum, suggesting that IL-17–producing cells contribute to atypical disease but do not determine its location... In agreement with past reports, however, transferring mixed populations of IFNγ- and IL-17–producing cells resulted in a mixed disease phenotype, with increasing numbers of IFNγ producers causing progressively more spinal cord disease... Why IFNγ induces inflammation in one tissue and not another remains unknown—particularly because no obvious regional differences in the expression of the receptor were detected... The authors suspect that IFNγ triggers a localized production of T cell–attracting chemokines in the spine.

No MeSH data available.


Inflammation (arrows) is focused on the cerebellum, not the spine, in mice lacking the IFNγ receptor.
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fig1: Inflammation (arrows) is focused on the cerebellum, not the spine, in mice lacking the IFNγ receptor.


Friend to the brain, foe to the spine
Inflammation (arrows) is focused on the cerebellum, not the spine, in mice lacking the IFNγ receptor.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2571917&req=5

fig1: Inflammation (arrows) is focused on the cerebellum, not the spine, in mice lacking the IFNγ receptor.

View Article: PubMed Central

AUTOMATICALLY GENERATED EXCERPT
Please rate it.

Regional responses to interferon-γ (IFNγ) dictated whether the spinal cord or cerebellum came under fire in mice with EAE, a mouse model of human multiple sclerosis (MS)... In classical EAE, the T cell attack is focused on the spinal cord... But in atypical disease, the cerebellum and brain stem are the primary victims... A prior study suggested that the ratio of interleukin (IL)-17 to IFNγ determines whether disease pathology occurs in the spine or brain, with increasing levels of IL-17 associated with disease in the brain... But when transferred into mice lacking the IFNγ receptor, the cells instead attacked the cerebellum and brain stem, sparing the spinal cord... The production of IL-17 by the transferred T cells was comparable in both settings... However, the production of IL-17 by non-T cells predominated in the cerebellum, suggesting that IL-17–producing cells contribute to atypical disease but do not determine its location... In agreement with past reports, however, transferring mixed populations of IFNγ- and IL-17–producing cells resulted in a mixed disease phenotype, with increasing numbers of IFNγ producers causing progressively more spinal cord disease... Why IFNγ induces inflammation in one tissue and not another remains unknown—particularly because no obvious regional differences in the expression of the receptor were detected... The authors suspect that IFNγ triggers a localized production of T cell–attracting chemokines in the spine.

No MeSH data available.