MGL/CLEC10A is an important C-type lectin receptor activated in the innate immune response to <i>Mycobacterium tuberculosis</i> and is suppressed in people with HIV.

ABSTRACT: Mycobacterium tuberculosis (Mtb) and HIV are leading infectious causes of death worldwide and act synergistically to worsen disease during co-infection. C-type lectin receptors (CLR) respond to pathogen-associated carbohydrates to activate downstream innate immunity and can be exploited for entry of intracellular pathogens. The macrophage (MΦ) galactose-type lectin (MGL, CLEC10A) is an immunomodulatory CLR associated with M2 MΦ. We previously described an immune role for a murine MGL homologue in an experimental model of tuberculosis (TB). Herein we extend these findings by identifying human MGL as an important member of the Mtb-responsive pathogen recognition receptor (PRR) repertoire that is activated in both M1 and M2 polarizing conditions. MΦ exposure to Mtb activates MGL expres

SUBMITTER: Browning SE 

PROVIDER: S-EPMC12522201 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature