The abstract is read at the publisher; the summary is JClub's.
TREM2 activation with 4D9 increases fibrous cap formation in low allele burden Jak2V617F atherosclerosis by boosting macrophage PDGFB and stromal PDGFRβ signaling.
- Why it matters: In Jak2V617F clonal hematopoiesis, inflammatory signaling suppresses macrophage TREM2 and is linked to plaque instability, but the PDGF-dependent stromal mechanism behind TREM2 agonism was unclear.
- What they did: In LAB Jak2V617F mice, macrophage Pdgfb was deleted in CX3CR1-lineage cells or stromal Pdgfra was deleted in Col1a2-lineage fibroblast-enriched cells, then plaque composition and stromal populations were assessed after 4D9 treatment.
- The result: Pdgfb deletion markedly reduced 4D9-driven increases in fibrous cap area and lesional PDGFRβ+ cells, while Pdgfra deletion abolished the fibrous cap response; single-cell RNA-seq showed 4D9 expanded Fmod+ and CD26/Dpp4+ fibroblasts, with CD26+ fibroblasts linked to reduced macrophage migration programs and DPP4-dependent chemotaxis effects.
The findingWhy it mattersWhat they didThe result
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