Steven J. Bensinger

SCD-dependent lipid metabolism licenses alternative macrophage activation and macrophage plasticity

This study identifies SCD as a lipid metabolic checkpoint that regulates macrophage activation and plasticity by maintaining lipid desaturation balance and preventing pro-inflammatory responses.

SCD1 and SCD5 Modulate PARP-Dependent DNA Repair via Fatty Acid Desaturation in Glioblastoma

This study shows SCD1 and SCD5 modulate DNA repair in glioblastoma via fatty acid desaturation, with SCD5 specifically affecting sphingolipids and PARP1 activity.

TREM2+ macrophages accumulate in alveoli of human pulmonary tuberculosis providing a permissive niche for bacterial growth

This study identifies TREM2+ lipid-laden macrophages in alveolar TB pneumonia that support Mtb survival, contrasting with granulomas, and shows pharmacological reversal of this immunometabolic state.

Targeting SCD triggers lipotoxicity of cancer cells and enhances anti-tumor immunity in breast cancer brain metastasis mouse models

This study shows that inhibiting SCD in breast cancer brain metastases induces lipotoxicity and enhances anti-tumor immunity, improving survival in mouse models.

Pro-inflammatory macrophage activation does not require inhibition of mitochondrial respiration

This study shows that reduced oxidative phosphorylation is not required for pro-inflammatory macrophage activation, challenging the conventional model of mitochondrial reprogramming.

Flow-Mediated Modulation of the Endothelial Cell Lipidome

This study examines how different blood flow patterns alter the lipidome of human aortic endothelial cells and identifies stimulus-specific lipid reprogramming in response to pro-inflammatory agonists.

IL-4 Licenses B Cell Activation Through Cholesterol Synthesis

This study shows IL-4 promotes B cell activation by upregulating cholesterol synthesis, which is essential for ER expansion, cell cycle progression, and proliferation during influenza infection.

Combined Treatment with Dopamine Receptor Antagonists and Radiation Creates a Metabolic Vulnerability in Mouse Models of Glioblastoma

This study shows that combining quetiapine, atorvastatin, and radiation extends survival in glioblastoma mouse models by exploiting a metabolic vulnerability.