ArticleBrain, behavior, and immunity2011
IL-10 within the CNS is necessary for CD4+ T cells to mediate neuroprotection.
Article in Brain, behavior, and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Selection and Prioritization of Candidate Drug Targets for Amyotrophic Lateral Sclerosis Through a Meta-Analysis Approach.Journal of molecular neuroscience : MN · 2017Pooled it
- Identification of Comprehensive Landscape of Peripheral Immunity and Chemokine-Related Genes in Amyotrophic Lateral Sclerosis.ImmunoTargets and therapy · 2026Article
- Thoracic Spinal Cord Contusion Impacts on Lumbar Enlargement: Molecular Insights.Molecular neurobiology · 2025Article
- Optogenetic Activation of Astrocytes Reduces Blood-Brain Barrier Disruption via IL-10 In Stroke.Aging and disease · 2023Article
- Pre-Clinical Assessment of Roflumilast Therapy in a Thoracic Model of Spinal Cord Injury.Pharmaceutics · 2023Article
- Central Facial Nervous System Biomolecules Involved in Peripheral Facial Nerve Injury Responses and Potential Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2023Review
- Cellular Sources and Neuroprotective Roles of Interleukin-10 in the Facial Motor Nucleus after Axotomy.Cells · 2022Article
- Infiltration Profile of Regulatory T Cells in Osteoarthritis-Related Pain and Disability.Biomedicines · 2022Article
- The Role of Microglia in Neuroinflammation of the Spinal Cord after Peripheral Nerve Injury.Cells · 2022Review
- Astrocyte-targeted Overproduction of IL-10 Reduces Neurodegeneration after TBI.Experimental neurobiology · 2022Article
- Modulation of astrocyte phenotype in response to T-cell interaction.Journal of neuroimmunology · 2021Article
- Deletion of CD38 and supplementation of NADScientific reports · 2020Article
- CD4+ T cell expression of the IL-10 receptor is necessary for facial motoneuron survival after axotomy.Journal of neuroinflammation · 2020Article
- Biology and therapeutic potential of interleukin-10.The Journal of experimental medicine · 2020Review
- Use of a Combination Strategy to Improve Morphological and Functional Recovery in Rats With Chronic Spinal Cord Injury.Frontiers in neurology · 2020Article
- Sustained interleukin-10 delivery reduces inflammation and improves motor function after spinal cord injury.Journal of neuroinflammation · 2019Article
- T Cells as an Emerging Target for Chronic Pain Therapy.Frontiers in molecular neuroscience · 2019Article
- Resolution of inflammation-induced depression requires T lymphocytes and endogenous brain interleukin-10 signaling.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- The Interleukin-10 Family of Cytokines and Their Role in the CNS.Frontiers in cellular neuroscience · 2018Review
- A neuroprotective astrocyte state is induced by neuronal signal EphB1 but fails in ALS models.Nature communications · 2017Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
We have previously shown that immunodeficient mice exhibit significant facial motoneuron (FMN) loss compared to wild-type (WT) mice after a facial nerve axotomy. Interleukin-10 (IL-10) is known as a regulatory cytokine that plays an important role in maintaining the anti-inflammatory environment within the central nervous system (CNS). IL-10 is produced by a number of different cells, including Th2 cells, and may exert an anti-apoptotic action on neurons directly. In the present study, the role of IL-10 in mediating neuroprotection following facial nerve axotomy in Rag-2- and IL-10-deficient mice was investigated. Results indicate that IL-10 is neuroprotective, but CD4+ T cells are not the requisite source of IL-10. In addition, using real-time PCR analysis of laser microdissected brainstem sections, results show that IL-10 mRNA is constitutively expressed in the facial nucleus and that a transient, significant reduction of IL-10 mRNA occurs following axotomy under immunodeficient conditions. Dual labeling immunofluorescence data show, unexpectedly, that the IL-10 receptor (IL-10R) is constitutively expressed by facial motoneurons, but is selectively induced in astrocytes within the facial nucleus after axotomy. Thus, a non-CD4+ T cell source of IL-10 is necessary for modulating both glial and neuronal events that mediate neuroprotection of injured motoneurons, but only with the cooperation of CD4+ T cells, providing an avenue of novel investigation into therapeutic approaches to prevent or reverse motoneuron diseases, such as amyotrophic lateral sclerosis (ALS).
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