Immune-mediated neuroprotection of axotomized mouse facial motoneurons is dependent on the IL-4/STAT6 signaling pathway in CD4+ T cells

DeBoy, Cynthia A.; Xin, Junping; Byram, Susanna C.; Serpe, Craig J.; Sanders, Virginia M.; Jones, Kathryn J.

doi:10.1016/j.expneurol.2006.04.028

Cited by 63 publications

(71 citation statements)

References 81 publications

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“…Adenoviralmediated IL-4 or IL-10 expression enhances the survival of axotomized retinal ganglion cells through the inhibition of NO synthesis (Koeberle et al, 2004). Th2 cells promote facial motoneuron survival after facial nerve axotomy, but a reduced survival rate has been reported in IL-4 knock-out mice (Deboy et al, 2006). More severe secondary inflammatory responses have been reported in IL-10 knock-out mice, resulting in worse functional recovery after spinal cord compression (Genovese et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Acid Fibroblast Growth Factor and Peripheral Nerve Grafts Regulate Th2 Cytokine Expression, Macrophage Activation, Polyamine Synthesis, and Neurotrophin Expression in Transected Rat Spinal Cords

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Acid Fibroblast Growth Factor and Peripheral Nerve Grafts Regulate Th2 Cytokine Expression, Macrophage Activation, Polyamine Synthesis, and Neurotrophin Expression in Transected Rat Spinal Cords

et al. 2011

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“…As statistical analysis revealed that the distribution of the data was not normal, Spearman's rank correlation analysis was used to determine the relationship between T cells and neuronal death (as measured by the number of microglial phagocytic clusters). For neuronal cell counts, facial motor neurons were quantified in 8 representative sections of the FMN, as described previously (Deboy et al, 2006;Ha et al, 2007a). The medial nucleus, which receives innervation from the auricular branch of the facial nerve, remained uninjured and thus was excluded from the analysis.…”

Section: Quantification and Statistical Analysismentioning

confidence: 99%

Influence of injury severity on the rate and magnitude of the T lymphocyte and neuronal response to facial nerve axotomy

Ha¹,

Parikh²,

Huang³

et al. 2008

Journal of Neuroimmunology

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The temporal relationship between severity of peripheral axonal injury and T lymphocyte trafficking to the neuronal cell bodies of origin in the brain has been unclear. We sought to test the hypothesis that greater neuronal death induced by disparate forms of peripheral nerve injury would result in differential patterns of T cell infiltration and duration at the cell bodies of origin in the brain and that these measures would correlate with the magnitude of neuronal death over time and cumulative neuronal loss. To test this hypothesis, we compared the time course of CD3 + T cell infiltration and neuronal death (assessed by CD11b + perineuronal microglial phagocytic clusters) following axonal crush versus axonal resection injuries, two extreme variations of facial nerve axotomy that result in mild versus severe neuronal loss, respectively, in the facial motor nucleus. We also quantified the number of facial motor neurons present at 49 days post-injury to determine whether differences in the levels of neuronal death between nerve crush and resection correlated with differences in cumulative neuronal loss. Between 1-7 days post-injury when levels of neuronal death were minimal, we found that the rate of accumulation and magnitude of the T cell response was similar following nerve crush and resection. Differences in the T cell response were apparent by 14 days post-injury when the level of neuronal death following resection was substantially greater than that seen in crush injury. For nerve resection, the peak of neuronal death at 14 days post-resection was followed by a maximal T cell response one week later at 21 days. Differences in the level of neuronal death between the two injuries across the time course tested reflected differences in cumulative neuronal loss at 49 days post-injury. Altogether, these data suggest that the trafficking of T cells to the injured FMN is dependent upon the intensity of peripheral nerve injury and associated neuronal death.

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“…More recent data from these investigators suggest that regulatory T cells (CD4+CD25+ T cells) do not play a role in FMN neuroprotection (Deboy et al, 2006a), but that the IL-4/STAT-6 pathway (Th2 cells) is required for motor neuron survival (Deboy et al, 2006b). Is there a particular population of phenotypically distinct CD4 + T cells that mediate neuroprotection?…”

Section: Theme 4 Neuroprotective Effect Of T Cellsmentioning

confidence: 99%

Brain behavior and immunity: Twenty years of T cells

Moynihan

2007

Brain, Behavior, and Immunity

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During the period from 1987-2007, our understanding of nervous system-T lymphocyte bidirectional communication advanced exponentially. Progress in exploring these relationships was aided by the constant development of new, cutting-edge technologies, and by a steady growth in interest, and number, of scientists who recognized the need to conduct cross-disciplinary research. In this brief review of 20 years of Brain, Behavior, and Immunity (BBI), we highlight just a small number of the important studies published in the journal that collectively have provided the foundation for our current understanding of brain, behavior, and, specifically, T cells.

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Immune-mediated neuroprotection of axotomized mouse facial motoneurons is dependent on the IL-4/STAT6 signaling pathway in CD4+ T cells

Cited by 63 publications

References 81 publications

Acid Fibroblast Growth Factor and Peripheral Nerve Grafts Regulate Th2 Cytokine Expression, Macrophage Activation, Polyamine Synthesis, and Neurotrophin Expression in Transected Rat Spinal Cords

Acid Fibroblast Growth Factor and Peripheral Nerve Grafts Regulate Th2 Cytokine Expression, Macrophage Activation, Polyamine Synthesis, and Neurotrophin Expression in Transected Rat Spinal Cords

Influence of injury severity on the rate and magnitude of the T lymphocyte and neuronal response to facial nerve axotomy

Brain behavior and immunity: Twenty years of T cells

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