ArticleFrontiers in immunology2020
Triggering Receptor Expressed on Myeloid Cell 2 R47H Exacerbates Immune Response in Alzheimer's Disease Brain.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Type-1 interferons associated with microglial-mediated neuroinflammation in Alzheimer's disease.Journal of neuroinflammation · 2026Review
- Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026Review
- Inactivation of the PHD3-FOXO3 axis blunts the type I interferon response in microglia and ameliorates Alzheimer's disease progression.Science advances · 2025Article
- Interferon Regulatory Factors as a Potential Therapeutic Target for Neuroinflammation: A Focus on Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Unraveling the Complex Interplay Between Neuroinflammation and Depression: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Article
- TREM2 variants that cause early dementia and increase Alzheimer's disease risk affect gene splicing.Brain : a journal of neurology · 2024Article
- Article
- MAD-microbial (origin of) Alzheimer's disease hypothesis: from infection and the antimicrobial response to disruption of key copper-based systems.Frontiers in neuroscience · 2024Review
- Genetic Phenotypes of Alzheimer's Disease: Mechanisms and Potential Therapy.Phenomics (Cham, Switzerland) · 2023Review
- Role of neuroinflammation in neurodegeneration development.Signal transduction and targeted therapy · 2023Review
- Defects in lysosomal function and lipid metabolism in human microglia harboring a TREM2 loss of function mutation.Acta neuropathologica · 2023Article
- Article
- Role of anthraquinones in combating insulin resistance.Frontiers in pharmacology · 2023Review
- Article
- Concerted type I interferon signaling in microglia and neural cells promotes memory impairment associated with amyloid β plaques.Immunity · 2022Article
- Non-Communicable Neurological Disorders and Neuroinflammation.Frontiers in immunology · 2022Review
- AD-linked R47H-Science translational medicine · 2021Article
- Novel TREM2 splicing isoform that lacks the V-set immunoglobulin domain is abundant in the human brain.Journal of leukocyte biology · 2021Article
- Delivery Platforms for CRISPR/Cas9 Genome Editing of Glial Cells in the Central Nervous System.Frontiers in genome editing · 2021Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
The R47H variant in the microglial triggering receptor expressed on myeloid cell 2 (TREM2) receptor is a strong risk factor for Alzheimer's disease (AD). To characterize processes affected by R47H, we performed an integrative network analysis of genes expressed in brains of AD patients with R47H, sporadic AD without the variant, and patients with polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL), systemic disease with early-onset dementia caused by loss-of-function mutations in TREM2 or its adaptor TYRO protein tyrosine kinase-binding protein (TYROBP). Although sporadic AD had few perturbed microglial and immune genes, TREM2 R47H AD demonstrated upregulation of interferon type I response and pro-inflammatory cytokines accompanied by induction of NKG2D stress ligands. In contrast, PLOSL had distinct sets of highly perturbed immune and microglial genes that included inflammatory mediators, immune signaling, cell adhesion, and phagocytosis. TREM2 knockout (KO) in THP1, a human myeloid cell line that constitutively expresses the TREM2- TYROBP receptor, inhibited response to the viral RNA mimetic poly(I:C) and phagocytosis of amyloid-beta oligomers; overexpression of ectopic TREM2 restored these functions. Compared with wild-type protein, R47H TREM2 had a higher stimulatory effect on the interferon type I response signature. Our findings point to a role of the TREM2 receptor in the control of the interferon type I response in myeloid cells and provide insight regarding the contribution of R47H TREM2 to AD pathology.
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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.