Key result
Targeting macrophage CD40-TRAF6 signaling with TRAF-STOPs reduces atherosclerosis in mice.
Why the study?
Does TRAF-STOP treatment reduce atherosclerosis in mice?
Does TRAF-STOP treatment reduce atherosclerosis in mice?
Targeting CD40-TRAF6 signaling in macrophages using TRAF-STOPs reduces atherosclerosis in preclinical models while potentially avoiding broad immune suppression.
BACKGROUND: Disrupting the costimulatory CD40-CD40L dyad reduces atherosclerosis, but can result in immune suppression. The authors recently identified small molecule inhibitors that block the interaction between CD40 and tumor necrosis factor receptor-associated factor (TRAF) 6 (TRAF-STOPs), while leaving CD40-TRAF2/3/5 interactions intact, thereby preserving CD40-mediated immunity. OBJECTIVES: This study evaluates the potential of TRAF-STOP treatment in atherosclerosis. METHODS: ) mice. Recombinant high-density lipoprotein (rHDL) nanoparticles were used to target TRAF-STOPs to macrophages. RESULTS: mice. CONCLUSIONS: TRAF-STOPs can overcome the current limitations of long-term CD40 inhibition in atherosclerosis and have the potential to become a future therapeutic for atherosclerosis.
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Seijkens et al. (2018) studied Atherosclerosis. TRAF-STOPs was evaluated. Targeting CD40-induced TRAF6 signaling in macrophages using TRAF-STOPs reduces atherosclerosis in mice, offering a potential therapeutic strategy.
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