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r47h
363 studies tagged r47h, dated 2000-05-01 to 2026-06-02. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Gain-of-function Modulation of TREM2 and its Impact on Amyloid-β and Tau Pathologies in Alzheimer's Disease: A Systematic Review and Meta-analysis of Animal Studies 2026-06-02
- The TREM2 agonistic antibody AL002 in early Alzheimer's disease: a phase 2 randomized trial 2026-03-05
- Decoding TREM2 Signaling Pathways 2026-01-09
Studies
363 studies carry this tag.
Date range
2000 to 2026
Top journals
- Molecular neurodegeneration 26
- Neurobiology of aging 16
- Neuron 10
- The Journal of experimental medicine 10
- Acta neuropathologica 9
147 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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In multiple sclerosis, inflammation can successfully be prevented, while promoting repair is still a major challenge.
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While there is a strong evidence for neural tissue destruction mediated by adaptive autoimmune responses, it is still debated how innate immune responses contribute to neuroinflammatory and neurodegenerative diseases such as multiple sclerosis and Alzheimer's disease.
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The triggering receptor expressed on myeloid cells 2 (TREM-2) delivers intracellular signals through the adaptor DAP12 to regulate myeloid cell function both within and outside the immune system.
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DAP12 is an ITAM-containing adapter that associates with receptors in myeloid and NK cells.
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These results provide new evidence that TREM2 regulates OC function independent of its effects on multinucleated OC differentiation.
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Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL) is a recessively inherited disease characterized by early onset dementia associated with bone cysts.
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Together with its adaptor protein, the adaptor protein of 12 kDa also known as KARAP and TYROBP (DAP12), triggering receptor expressed in myeloid cells 2 (TREM2) is a stimulatory membrane receptor of the immunoglobulin/lectin-like superfamily, well known in myeloid cells.
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52/100
Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL), Nasu-Hakola disease, is a globally distributed recessively inherited disease.
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We recently described the cloning of murine triggering receptor expressed by myeloid cells (TREM) 2, a single Ig domain DNAX adaptor protein 12-associated receptor expressed by cells of the myeloid lineage.
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Triggering receptors expressed by myeloid cells (TREMs) belong to a rapidly expanding family of receptors that include activating and inhibitory isoforms encoded by a gene cluster linked to the MHC.
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We have characterized a cluster of single immunoglobulin variable (IgV) domain receptors centromeric of the major histocompatibility complex (MHC) on human chromosome 6.
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Microglial activation is an early and common feature of almost all neuropathologies, including multiple sclerosis, Alzheimer's disease and mechanical injury.
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We have identified new activating receptors of the Ig superfamily expressed on human myeloid cells, called TREM (triggering receptor expressed on myeloid cells).
From across this tag
8 of the 363 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 8. The same 8 appear here every time.
- TREM2 and the neuroimmunology of Alzheimer's disease
- Prior activation state shapes the microglia response to antihuman TREM2 in a mouse model of Alzheimer's disease
- TREM2 protects against cerebral ischemia/reperfusion injury
- Soluble TREM2 induces inflammatory responses and enhances microglial survival
- LILRB2-mediated TREM2 signaling inhibition suppresses microglia functions
- TREM2 deficiency reprograms intestinal macrophages and microbiota to enhance anti-PD-1 tumor immunotherapy
- Soluble TREM2 changes during the clinical course of Alzheimer's disease: A meta-analysis
- TREM2 is upregulated in amyloid plaque-associated microglia in aged APP23 transgenic mice