ArticlePloS one2014
A lack of immune system genes causes loss in high frequency hearing but does not disrupt cochlear synapse maturation in mice.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- Complement factor B is essential for the proper function of the peripheral auditory system.Frontiers in neurology · 2023Article
- Heterogeneity in macrophages along the cochlear spiral in mice: insights from SEM and functional analyses.Frontiers in cellular neuroscience · 2023Article
- Cochlear Immune Response in Presbyacusis: a Focus on Dysregulation of Macrophage Activity.Journal of the Association for Research in Otolaryngology : JARO · 2022Review
- Macrophages Are Dispensable for Postnatal Pruning of the Cochlear Ribbon Synapses.Frontiers in cellular neuroscience · 2021Article
- Interactions between Macrophages and the Sensory Cells of the Inner Ear.Cold Spring Harbor perspectives in medicine · 2019Review
- TSP1 and TSP2 Have Unique and Overlapping Roles in Protecting against Noise-Induced Auditory Synaptopathy.Neuroscience · 2019Article
- Characterization of Wnt and Notch-Responsive Lgr5+ Hair Cell Progenitors in the Striolar Region of the Neonatal Mouse Utricle.Frontiers in molecular neuroscience · 2018Article
- Macrophage-Mediated Glial Cell Elimination in the Postnatal Mouse Cochlea.Frontiers in molecular neuroscience · 2017Article
- Facial Nerve Recovery in KbDb and C1q Knockout Mice: A Role for Histocompatibility Complex 1.Plastic and reconstructive surgery. Global open · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Early cochlear development is marked by an exuberant outgrowth of neurites that innervate multiple targets. The establishment of mature cochlear neural circuits is, however, dependent on the pruning of inappropriate axons and synaptic connections. Such refinement also occurs in the central nervous system (CNS), and recently, genes ordinarily associated with immune and inflammatory processes have been shown to play roles in synaptic pruning in the brain. These molecules include the major histocompatibility complex class I (MHCI) genes, H2-K(b) and H2-D(b), and the complement cascade gene, C1qa. Since the mechanisms involved in synaptic refinement in the cochlea are not well understood, we investigated whether these immune system genes may be involved in this process and whether they are required for normal hearing function. Here we report that these genes are not necessary for normal synapse formation and refinement in the mouse cochlea. We further demonstrate that C1qa expression is not necessary for normal hearing in mice but the lack of expression of H2-K(b) and H2-D(b) causes hearing impairment. These data underscore the importance of the highly polymorphic family of MHCI genes in hearing in mice and also suggest that factors and mechanisms regulating synaptic refinement in the cochlea may be distinct from those in the CNS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.