ArticleNature communications2014
MHC-I expression renders catecholaminergic neurons susceptible to T-cell-mediated degeneration.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02939534 (Antigen Presentation and Lymphocyte Response in Parkinson's Disease), which is not on this map. Cited by 207 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Antigen Presentation and Lymphocyte Response in Parkinson's Disease
Who cites it
207 citing papers in PubMed, 331 citations in OpenAlex.
- The Impact of Antigen Presentation on BBB Disruption and Neuroinflammation.Physiology (Bethesda, Md.) · 2026Review
- Neuroinflammation in Alzheimer's and Parkinson's diseases: pathogenic mechanisms and therapeutic strategies.Translational neurodegeneration · 2026Review
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- Role of aging‑related cytokines in neurodegenerative disease (Review).International journal of molecular medicine · 2026Review
- The vicious cycle: unraveling the interplay between α-synuclein, mitochondrial dysfunction, and neuroinflammation in Parkinson's disease.Journal of neurology · 2026Review
- Reevaluating the role of beta2-microglobulin: new insights on selective vulnerability in ALS pathology.Acta neuropathologica · 2026Article
- Cytotoxic T cell recognition of α-synuclein drives pathogenic immune responses in multiple system atrophy.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Misfolded Proteins and Cognitive Decline: Mechanistic Insights into Neurodegenerative Disorders.Neurology international · 2026Review
- The immunoproteasome as a neuroimmune hub in the central nervous system: from proteostasis stress to inflammatory pathology.Journal of neuroinflammation · 2026Review
- Hippocampal neuronal hypoexcitability contributes to PTSD-like phenotypes in the experimental autoimmune encephalomyelitis model.Frontiers in psychiatry · 2026Article
- Association between Alzheimer's disease and MHC-I antigen processing and presentation pathway: a narrative review.Frontiers in immunology · 2026Review
- Neuroinflammation and metabolic reprogramming in Parkinson's disease.Frontiers in immunology · 2026Review
- Revisiting the alpha-synuclein paradox in melanoma-Parkinson's disease connection: more than a tale of two cell fates.Cellular and molecular life sciences : CMLS · 2025Review
- Helicobacter pylori infection and α-synuclein pathology drive parallel neurodegenerative pathways in the substantia nigra.Journal of neuroinflammation · 2025Article
- Patient-Derived Neurons Exhibit α-Synuclein Pathology and Previously Unrecognized Major Histocompatibility Complex Class I Elevation in Mitochondrial Membrane Protein-Associated Neurodegeneration.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Review
- Glycosylation in neuroinflammation: mechanisms, implications, and therapeutic strategies for neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Transgenic inducible MHC I overexpression in mouse alveolar type 2 cells.Transgenic research · 2025Article
- Changes in Neuroimmunological Synapses During Cerebral Ischemia.Translational stroke research · 2025Review
- Neurological Complications in Inborn Errors of Immunity: A Scoping Review of Clinical Spectrum, Pathophysiological Mechanisms, and Therapeutic Strategies.Clinical reviews in allergy & immunology · 2025Article
147 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
Abstract
Subsets of rodent neurons are reported to express major histocompatibility complex class I (MHC-I), but such expression has not been reported in normal adult human neurons. Here we provide evidence from immunolabel, RNA expression and mass spectrometry analysis of postmortem samples that human catecholaminergic substantia nigra and locus coeruleus neurons express MHC-I, and that this molecule is inducible in human stem cell-derived dopamine (DA) neurons. Catecholamine murine cultured neurons are more responsive to induction of MHC-I by gamma-interferon than other neuronal populations. Neuronal MHC-I is also induced by factors released from microglia activated by neuromelanin or alpha-synuclein, or high cytosolic DA and/or oxidative stress. DA neurons internalize foreign ovalbumin and display antigen derived from this protein by MHC-I, which triggers DA neuronal death in the presence of appropriate cytotoxic T cells. Thus, neuronal MHC-I can trigger antigenic response, and catecholamine neurons may be particularly susceptible to T-cell-mediated cytotoxic attack.
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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.