Joseph Keane

This study identifies increased glycolysis in SLE neutrophil subsets, correlating with disease activity and metabolic flexibility.

This study shows HIV-1 infection suppresses Mtb-induced glycolytic reprogramming in macrophages, altering immunometabolic responses and increasing TB susceptibility.

This study shows human macrophages secrete both interferon α and β during Mtb infection, challenging previous assumptions about their kinetics and timing.

This study compares monocyte phenotypes, function, and metabolism in latent TB infection, active TB disease, and healthy controls, finding distinct metabolic and cytokine profiles that differentiate the conditions.

This study identifies sex-specific metabolic differences in human neutrophil subsets, showing male low-density neutrophils have higher oxidative and glycolytic activity compared to female counterparts, independent of maturity.

This study identifies mitochondrial bioenergetic failure in SLE immunocytes, showing reduced OXPHOS across multiple immune subsets and proposes targeting mitochondrial fitness for therapy.

This study shows dexamethasone reduces glycolysis in human macrophages but enhances mycobacterial killing, suggesting a potential therapeutic benefit in tuberculosis.

The paper identifies mitochondrial metabolism as a key regulator of phagocytic function in human lung monocytes and macrophages, showing that succinate supplementation enhances these functions and promotes macrophage differentiation.

This study shows that human airway macrophages reprogram their metabolism in response to IFN-γ, leading to glycolysis-dependent functional plasticity that differs from monocyte-derived macrophages.

The paper shows that mycobacteria use phenolic glycolipid (PGL) to escape resident macrophages by activating the STING pathway and recruiting monocytes, suggesting PGL-blocking interventions could prevent tuberculosis.