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TREM and TREM-like receptors in inflammation and disease
Open accessAbstract
Since the discovery of triggering receptor expressed on myeloid cells (TREM)-1 in 2000, evidence documenting the profound ability of the TREM and TREM-like receptors to regulate inflammation has rapidly accumulated. Monocytes, macrophages, myeloid dendritic cells, plasmacytoid dendritic cells, neutrophils, microglia, osteoclasts, and platelets all express at least one member of the TREM family, underscoring the importance of these proteins in the regulation of innate resistance. Recent work on the TREM family includes: characterization of a new receptor expressed on plasmacytoid dendritic cells; definition of a key role for TREM in inflammatory bowel disease and multiple sclerosis; an expanded list of diseases associated with the release of soluble forms of TREM proteins; and identification of the first well characterized TREM ligand: B7-H3, a ligand for TREM-like Transcript (TLT)-2. Moreover, analysis of TREM signaling has now identified key regulatory components and defined pathways that may be responsible for the complex functional interactions between the TREM and toll-like receptors. In addition, there is expanding evidence of a role for TREM in the regulation of integrin function via Plexin-A1. Together these new findings define the TREM and TREM-like receptors as pluripotent modifiers of disease through the integration of inflammatory signals with those associated with leukocyte adhesion.
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Humans with TREM2 deficiency develop Nasu-Hakola syndrome, characterised by dementia and bone cysts.
“Humans with TREM2 deficiency develop the Nasu-Hakola syndrome, characterised by dementia and bone cysts [106]”
From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [106]
PLCγ2 belongs to the same interaction network as TREM2 and may be directly involved in TREM2 signaling.
“PLCγ2 belongs to the same interaction network as TREM2 [6] and may be directly involved in its signaling pathway [15, 16].”
From Alzheimer’s disease phospholipase C-gamma-2 (PLCG2) protective variant is a functional hypermorph (2019) · cites this paper as [15]
The citation to this paper is attached to the suggestion that PLCγ2 may be involved in TREM2 signaling; the interaction-network statement has a separate citation. The TREM Signaling section describes TREM2 signaling through DAP12 and NTAL/LAB, but does not mention PLCγ2. Searches for “PLCγ2” and “phospholipase C gamma 2” found no passage connecting it to TREM2. (LLM, conf=0.73)
Experimental — accuracy not yet measuredDAP12 recruits the kinase Syk, which activates downstream mediators including PLC-gamma, PI-3K, and ERK.
“DAP12 recruits the protein tyrosine kinase Syk, which activates multiple downstream signaling mediators, including PLC-γ, PI-3K, and ERK (111, 112).”
From Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017) · cites this paper as [111]
TREM2 is a transmembrane glycoprotein expressed in myeloid cells that transmits intracellular signals through the adapters DAP12 and DAP10.
“TREM2 is transmembrane glycoprotein expressed in myeloid cells that transmits intracellular signals through two associated transmembrane adapters, DAP12 (also known as Tyrobp) and DAP10 (Hcst) (26, 111, 112).”
From Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017) · cites this paper as [111]
The BAC transgene design deletes essential exons in three other TREM-like genes, which have important innate immunity functions and may play distinct roles in AD.
“An important aspect of our BAC transgene design is the deletion of essential exons in three other TREM-like genes on the BAC, which are known to have important innate immunity function (Colonna, 2003; Ford and McVicar, 2009), and may play distinct roles in AD (Carrasquillo et al., 2017).”
From Elevated TREM2 Gene Dosage Reprograms Microglia Responsivity and Ameliorates Pathological Phenotypes in Alzheimer’s Disease Models (2018) · cites this paper as Ford and McVicar, 2009
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“TREM2 is a member of the triggering receptor expressed on myeloid (TREM) family, known to play a key role in modulating inflammation in the innate immune response [3].”
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GAO, X., DONG, Y., LIU, Z., & NIU, B. (2013) · Molecular Medicine Reports · doi:10.3892/mmr.2013.1268 · Cited by 60
Whittaker, G. C., Orr, S. J., Quigley, L., Hughes, L., Francischetti, I. M. B., Zhang, W., & McVicar, D. W. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.038398 · Cited by 33
Self-citationContributions of triggering-receptor-expressed-on-myeloid-cells-2 to neurological diseases
Han, J., Wang, M., Ren, M., & Lou, H. (2017) · International Journal of Neuroscience · doi:10.1080/00207454.2016.1264072 · Cited by 30
Metadata
- Authors
- Ford, J. W., & McVicar, D. W.
- Affiliations
- National Cancer Institute (US)
- Corresponding author
- McVicar, Daniel W
- ORCID
- McVicar, Daniel W
- Venue
- Current Opinion in Immunology
- Publisher
- Elsevier BV
- Published
- 2009-02
- Volume
- 21
- Issue
- 1
- Pages
- 38-46
- ISSN
- 0952-7915 (ISSN-L)
- PMC
- PMC2723941
- OpenAlex
- W2019558661
- Cited by
- 434
- References
- 60
- Citations by year
- 2026: 9 · 2025: 20 · 2024: 14 · 2023: 21 · 2022: 27 · 2021: 30 · 2020: 26 · 2019: 18 · 2018: 28 · 2017: 30 · 2016: 45 · 2015: 27 · 2014: 31 · 2013: 39 · 2012: 22
- FWCI
- 1.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (Z99 CA999999)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- TREM-1, TREM2, B7-H3, innate immunity, inflammation, inflammatory bowel disease, multiple sclerosis, plasmacytoid dendritic cells, monocytes, macrophages, microglia, neutrophils, osteoclasts, platelets, Toll-like receptors, PLXNA1, integrin function, leukocyte adhesion
- MeSH terms
- Triggering Receptor Expressed on Myeloid Cells-1, Animals, Autoimmune Diseases, Bacterial Infections, Cell Adhesion, Dendritic Cells, Gene Expression Regulation, Humans, Inflammation, Membrane Glycoproteins, Osteogenesis, Receptors, Immunologic, Signal Transduction, Antigens, CD, Receptor Cross-Talk, Feedback, Physiological, B7 Antigens
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