Cited by 17Nerve injury and regenerationFacial Nerve Paralysis Treatment and ResearchT-cell and B-cell Immunology

CD4+ T cell-mediated neuroprotection is independent of T cell-derived BDNF in a mouse facial nerve axotomy model

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Xin, Junping, Mesnard, Nichole A., Beahrs, Taylor, Wainwright, Derek A., Serpe, Craig J., Alexander, Thomas D., Sanders, Virginia M., Jones, Kathryn J.·2012·Brain, Behavior, and Immunity

Abstract

Background The production of neurotrophic factors, such as BDNF, has generally been considered an important mechanism of immune-mediated neuroprotection. However, the ability of T cells to produce BDNF remains controversial. Methods In the present study, we examined mRNA and protein of BDNF using RT-PCR and western blot, respectively, in purified and reactivated CD4(+) T cells. In addition, to determine the role of BDNF derived from CD4(+) T cells, the BDNF gene was specifically deleted in T cells using the Cre-lox mouse model system. Results Our results indicate that while both mRNA expression and protein secretion of BDNF in reactivated T cells were detected at 24 h, only protein could be detected at 72 h after reactivation. The results suggest a transient up-regulation of BDNF mRNA in reactivated T cells. Furthermore, in contrast to our hypothesis that the BDNF expression is necessary for CD4(+) T cells to mediate neuroprotection, mice with CD4(+) T cells lacking BDNF expression demonstrated a similar level of facial motoneuron survival compared to their littermates that expressed BDNF, and both levels were comparable to wild-type. The results suggest that the deletion of BDNF did not impair CD4(+) T cell-mediated neuroprotection. Conclusion Collectively, while CD4(+) T cells are a potential source of BDNF after nerve injury, production of BDNF is not necessary for CD4(+) T cells to mediate their neuroprotective effects.

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Crossref · 10.1016/j.bbi.2012.02.011

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  • Semax affected dendritic cells in rat cerebral hemisphere ischemia-damaged tissues.

    “In addition, Semax affected DCs, the presence of which in rat cerebral hemisphere ischemia-damaged tissues had been reported by other researchers [14].”

    From The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis (2014) · cites this paper as [14]

    The citation is attached to the reported presence of dendritic cells in ischemia-damaged rat cerebral tissue, rather than to Semax’s effect. The Introduction and Materials and Methods passages concern CD4+ T cells in a mouse facial nerve axotomy model; searches for dendritic cells, rat cerebral ischemia, and Semax found no passage addressing the cited point. Page numbers were not available in our copy. (LLM, conf=0.76)

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Authors
Xin, J., Mesnard, N. A., Beahrs, T., Wainwright, D. A., Serpe, C. J., Alexander, T. D., Sanders, V. M., & Jones, K. J.
Affiliations
  • Loyola University Medical Center (US)
  • University of Chicago (US)
  • Edward Hines, Jr. VA Hospital (US)
  • The Ohio State University (US)
  • Indiana University School of Medicine (US)
Corresponding author
Xin, Junping
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2012-08
Volume
26
Issue
6
Pages
886-890
ISSN
0889-1591 (ISSN-L)
OpenAlex
W2036691044
Cited by
17
References
19
Citations by year
2022: 1 · 2021: 1 · 2020: 2 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 5 · 2013: 3
FWCI
1.45
Type
journal article
Language
en
Open access
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • IUScholarWorks (Indiana University) (submittedVersion)
Funders
  • National Institutes of Health (NS40433)
  • Muscular Dystrophy Association (MDA202906)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
  • Health Sciences › Medicine › Neurology › Facial Nerve Paralysis Treatment and Research
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
CD4+ T cells, neuroprotection, brain-derived neurotrophic factor, nerve injury, facial nerve axotomy, facial motoneurons, T cell reactivation, Cre-loxP conditional knockout, neurotrophic factors
MeSH terms
Animals, Cell Count, Cell Survival, Female, Flow Cytometry, Motor Neurons, RNA, Blotting, Western, CD4-Positive T-Lymphocytes, Mice, Knockout, Brain-Derived Neurotrophic Factor, Axotomy, Facial Nerve Injuries, Mice, Real-Time Polymerase Chain Reaction

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