Galectins as Drivers of Host-Pathogen Dynamics in Mycobacterium tuberculosis Infection

Galectins form a protein family with a conserved carbohydrate-binding domain that specifically interacts with β-galactoside-containing glycoconjugates, which are found abundantly on mammalian cell surfaces. These proteins play crucial roles in various physiological and pathological processes including immune responses, cell adhesion, inflammation, and apoptosis. During tuberculosis infection, galectins exert diverse impacts on pathogenesis. The interaction between host and pathogen during TB involves intricate mechanisms influencing disease outcomes, where the pathogen exploits host glycosylation patterns to evade immune detection, underscoring the significant role of galectins in regulating these crucial host-pathogen interactions. Galectins facilitate pathogen recognition, enhance the phagocytosis of mycobacteria, support the formation of granuloma, and carefully balance the protective immunity against potential tissue damage. Additionally, galectins have an impact on the cytokine milieu by regulating the levels of pro-inflammatory cytokines and chemokines, essential for orchestrating granuloma formation and maintaining tuberculosis-associated homeostasis. This review delves into the intricate connection between galectins and tuberculosis; uncovering essential molecular mechanisms that deepen our understanding of how these proteins contribute to combating this pervasive infectious disease. Here we discuss the multifaceted roles that galectins play to uniquely and critically influence the core dynamics of host-pathogen interactions in tuberculosis.