Mutation-resolved single-cell transcriptomics reveals enhanced β-amyloid clearance in TET2-mutant human monocytes.
basic_science · Level V
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- Record sourced from PubMed, PMID 42635046.
- Also identified by DOI 10.1172/jci.insight.208804.
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Abstract
TET2-driven clonal hematopoiesis has been associated with reduced Alzheimer's disease risk, but mechanisms in humans remain unclear. Using mutation-resolved single-cell transcriptomics, we distinguished TET2-mutant and wild-type monocytes within the same aged individuals and identified enrichment of phagocytosis and complement programs in mutant cells. TET2 silencing in human monocytes and macrophages recapitulated this phenotype and enhanced β-amyloid uptake, indicating mutation-specific bias of innate immunity toward aggregate clearance.
Medical subject headings
- Monocytes
- Amyloid beta-Peptides
- DNA-Binding Proteins
- Proto-Oncogene Proteins
- Alzheimer Disease