Olivier Neyrolles

This study identifies CysK2 as a copper-responsive metabolic effector in M. tuberculosis that links copper sensing to redox homeostasis and intracellular adaptation during infection.

This study shows that type I interferon signaling in tuberculosis restricts T cell accumulation and motility by altering lung pathology and T cell states.

This study uses dual human lung models to evaluate anti-tuberculosis drugs and host-directed therapies, revealing compartment-specific efficacy and immune responses.

This study shows that inhibiting glycolysis in TB-infected macrophages reduces HIV-1 spread by blocking tunneling nanotubes and Siglec-1 expression.

This study identifies ST8SIA4-mediated polysialylation as essential for CCR2-driven monocyte egress from the bone marrow, revealing a novel regulatory mechanism in immune cell trafficking.

The paper shows HIV-1 Tat enhances Mtb and Toxoplasma growth by inhibiting clathrin-mediated endocytosis and autophagy through PI(4,5)P2 binding and palmitoylation.

The paper identifies RvD5-GPR32 signaling as a mechanism by which TB-PE reprograms macrophage metabolism to impair anti-tuberculous immunity.

This study identifies effluxosomes as dynamic membrane structures in M. tuberculosis that coordinate multi-metal resistance through PacL proteins and P-ATPase pumps.

The paper identifies a TUBB3+ cell population in TB granulomas across multiple species and patients, distinct from known cell types and present in other infections.

This study identifies MenT3 as a tRNA nucleotidyltransferase that modifies serine tRNAs in Mycobacterium tuberculosis, affecting bacterial growth and revealing its role in infection.

This study identifies LRP1 N-glycans with terminal galactoses as ligands for DCIR, revealing its specificity in immune regulation and potential therapeutic applications.

This study uses human airway organoids to model tuberculosis infection, showing mycobacteria infect epithelial cells with low efficiency and the organoid microenvironment controls but does not eliminate the pathogen.