Galectin{middle dot}3

Galectin-3 recruitment at the Mycobacterium tuberculosis-containing phagosome is critical in macrophage but dispensable in epithelial cells

Mycobacterium tuberculosis (Mtb) virulence relies in part on its ability to induce phagosomal membrane rupture, enabling bacterial access to the host cell cytosol. This process is largely mediated by the ESX{middle dot}1 secretion system, which is present in Mtb but absent from the vaccine strain BCG. Galectin{middle dot}3 (Gal3), a {beta}{middle dot}galactoside{middle dot}binding lectin, is recruited to damaged endomembranes and functions as a cytosolic sensor of membrane disruption.