SOD1G93A transgenic mouse CD4+ T cells mediate neuroprotection after facial nerve axotomy when removed from a suppressive peripheral microenvironment

@article{MesnardHoaglin2014SOD1G93ATM,
  title={SOD1G93A transgenic mouse CD4+ T cells mediate neuroprotection after facial nerve axotomy when removed from a suppressive peripheral microenvironment},
  author={Nichole A. Mesnard-Hoaglin and Junping Xin and Melissa Marie Haulcomb and Richard J. Batka and Virginia M. Sanders and Kathryn J Jones},
  journal={Brain, Behavior, and Immunity},
  year={2014},
  volume={40},
  pages={55-60}
}
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease involving motoneuron (MN) axonal withdrawal and cell death. Previously, we established that facial MN (FMN) survival levels in the SOD1(G93A) transgenic mouse model of ALS are reduced and nerve regeneration is delayed, similar to immunodeficient RAG2(-/-) mice, after facial nerve axotomy. The objective of this study was to examine the functionality of SOD1(G93A) splenic microenvironment, focusing on CD4(+) T cells, with… CONTINUE READING
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3 Excerpts

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