Immune cell-mediated neuroprotection is independent of estrogen action through estrogen receptor-alpha

Junping Xin, Keith N. Fargo, Lisa Tanzer, Virginia M. Sanders, Kathryn J. Jones

Research output: Contribution to journalArticle


It has been well documented that both estrogen and immune cells (CD4 + T cells) mediate neuroprotection in the mouse facial nerve axotomy model. Estrogen has been shown to play an important role in regulating the immune response. However, it is unclear whether immune cell-mediated neuroprotection is dependent on estrogen signaling. In this study, using FACS staining, we confirmed that the majority of CD4 + T cells express high levels of estrogen receptor-alpha (ERα), suggesting that CD4 + T cell-mediated neuroprotection may be modulated by estrogen signaling. We previously found that immunodeficient Rag-2KO mice showed a significant increase in axotomy-induced facial motoneuron death compared to immunocompetent wild-type mice. Therefore, we investigated axotomy-induced facial motoneuron loss in immunodeficient Rag-2KO mice that received 17β-estradiol treatment or adoptive transfer of immune cells from mice lacking functional ERα. Our results indicate that while estradiol treatment failed to rescue facial motoneurons from axotomy-induced cell death in Rag-2KO mice, immune cells lacking ERα successfully restored facial motoneuron survival in Rag-2 KO mice to a wild-type level. Collectively, we concluded that CD4 + T cell-mediated neuroprotection is independent of estrogen action through ERα.

Original languageEnglish (US)
Pages (from-to)23-28
Number of pages6
JournalMetabolic Brain Disease
Issue number1
StatePublished - Mar 1 2012


  • Axotomy
  • CD4 T cell
  • Estrogen
  • Facial motoneuron
  • Neuroprotection

ASJC Scopus subject areas

  • Clinical Neurology
  • Biochemistry
  • Cellular and Molecular Neuroscience

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