Jesse W. Williams

This study identifies TREM2's role in atherosclerosis regression by enhancing efferocytosis in lipid-experienced macrophages, suggesting TREM2 as a therapeutic target for plaque stabilization.

This study identifies C3aR as a mediator of HFD-induced hypothalamic microgliosis and obesity, showing its role in lipid droplet formation and neuroinflammation.

This study shows that CSF1R regulates monocyte differentiation and metabolism, with its blockade reducing Ly6Clow monocytes and affecting subset diversity through the hexosamine biosynthetic pathway.

The paper shows that both LynA and LynB restrict macrophage proliferation and drive TLR-induced ECM-remodeling and inflammatory cytokine production.

This study identifies conserved and tissue-specific transcriptional profiles of lipid-associated macrophages (LAMs) across species and inflammatory conditions using single-cell RNA sequencing.

The paper introduces MACanalyzeR, a scRNA-seq tool, to identify PPARγ-high lipid-associated macrophages in BAT that support thermogenic expansion.

The paper identifies CD226high macrophages derived from MDP monocytes as a new myeloid cell type involved in lipid metabolism regulation across tissues.

This study shows that a Trem2 agonist increases plaque macrophage survival and proliferation while improving plaque stability by enhancing collagen deposition and reducing necrotic core size.

This study shows that TREM2 loss increases parenchymal amyloid-beta but reduces cerebral amyloid angiopathy in Tg-SwDI mice.