Classical MHCI Molecules Regulate Retinogeniculate Refinement and Limit Ocular Dominance Plasticity
Open accessAbstract
Major histocompatibility complex class I (MHCI) genes were discovered unexpectedly in healthy CNS neurons in a screen for genes regulated by neural activity. In mice lacking just 2 of the 50+ MHCI genes H2-K(b) and H2-D(b), ocular dominance (OD) plasticity is enhanced. Mice lacking PirB, an MHCI receptor, have a similar phenotype. H2-K(b) and H2-D(b) are expressed not only in visual cortex, but also in lateral geniculate nucleus (LGN), where protein localization correlates strongly with synaptic markers and complement protein C1q. In K(b)D(b-/-) mice, developmental refinement of retinogeniculate projections is impaired, similar to C1q(-/-) mice. These phenotypes in K(b)D(b-/-) mice are strikingly similar to those in beta2 m(-/-)TAP1(-/-) mice, which lack cell surface expression of all MHCIs, implying that H2-K(b) and H2-D(b) can account for observed changes in synapse plasticity. H2-K(b) and H2-D(b) ligands, signaling via neuronal MHCI receptors, may enable activity-dependent remodeling of brain circuits during developmental critical periods.
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MHC class I molecules have been shown to be activity-dependent, localized to synapses, and co-localized with C1q.
“For example, MHC class I molecules, another class of immune molecules demonstrated to play a role in retinogeniculate pruning, have been shown to be activity-dependent, localized to synapses, and co-localized with C1q leaving the possibility that MHC class I molecules may play an upstream role in microglia-mediated pruning of synapses (Corriveau et al., 1998; Datwani et al., 2009; Goddard et al.,”
From Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner (2012) · cites this paper as Datwani et al., 2009
Many immune proteins have non-immune roles in the healthy nervous system, where they are required for normal neuronal development, dendritic morphology, and synaptic transmission.
“many immune proteins have non-immune roles in the healthy nervous system, where they are required for normal neuronal development, dendritic morphology, and synaptic transmission.”
From An innate immune response to adeno-associated virus genomes decreases cortical dendritic complexity and disrupts synaptic transmission (2024) · cites this paper as [20]
Proteins of the complement cascade (including C1q, C3, and C4) and members of MHCI (including H2-K and H2-D) contribute to synapse elimination in the developing visual system.
“proteins of the complement cascade (including C1q, C3, and C4) and members of MHCI (including H2-K and H2-D) contribute to synapse elimination in the developing visual system.20,21,22,23,24,25”
From An innate immune response to adeno-associated virus genomes decreases cortical dendritic complexity and disrupts synaptic transmission (2024) · cites this paper as [20]
A growing number of immune proteins have been identified that play central roles in neuronal homeostasis, where they negatively regulate neurite length, dendritic complexity, and synaptic transmission, and many are upregulated by TLR9.
“A growing number of immune proteins have been identified that play central roles in neuronal homeostasis, where they negatively regulate neurite length, dendritic complexity, and synaptic transmission,20,21,22,23,24,25,26,27,28,29,45,46,48,72,73,74,75,76,77,78,79 and many are upregulated by TLR9.”
From An innate immune response to adeno-associated virus genomes decreases cortical dendritic complexity and disrupts synaptic transmission (2024) · cites this paper as [20]
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References 46 · Cited by 212
- Authors
- Datwani, A., McConnell, M. J., Kanold, P. O., Micheva, K. D., Busse, B., Shamloo, M., Smith, S. J., & Shatz, C. J.
- Affiliations
- Stanford University (US)
- University of Maryland, College Park (US)
- Stanford Medicine (US)
- Corresponding author
- Shatz, Carla J.
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 64
- Issue
- 4
- Pages
- 463-470
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC2787480
- OpenAlex
- W2063781019
- Cited by
- 212
- References
- 46
- Citations by year
- 2025: 3 · 2024: 9 · 2023: 11 · 2022: 9 · 2021: 13 · 2020: 9 · 2019: 10 · 2018: 15 · 2017: 11 · 2016: 15 · 2015: 10 · 2014: 18 · 2013: 22 · 2012: 25
- FWCI
- 7.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1390 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R01 EY02858, R01 MH071666)
- G. Harold and Leila Y. Mathers Charitable Foundation (T32CA09361)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cognitive Neuroscience › Visual perception and processing mechanisms
- Keywords
- MHC class I, ocular dominance plasticity, H-2Kb, PirB, lateral geniculate nucleus, visual cortex, C1q, synaptic plasticity, beta2m, TAP1, critical period
- MeSH terms
- Animals, Animals, Newborn, Geniculate Bodies, H-2 Antigens, Mice, Inbred C57BL, Mice, Mutant Strains, Neuronal Plasticity, Retina, Visual Pathways, Neuroimmunomodulation, Mice, Knockout, Dominance, Ocular, Mice
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