Abstract
ABSTRACT Mannose-capped lipoarabinomannan (ManLAM) is a high molecular mass amphipathic lipoglycan identified in pathogenic Mycobacterium tuberculosis (M. tb) and M. bovis Bacillus Calmette-Guérin (BCG). ManLAM, serves as both an immunogen and a modulator of the host immune system, and its critical role in mycobacterial survival during infection has been well-characterized. ManLAM can be recognized by various types of receptors on both innate and adaptive immune cells, including macrophages, dendritic cells (DCs), neutrophils, natural killer T (NKT) cells, T cells and B cells. MamLAM has been shown to affect phagocytosis, cytokine production, antigen presentation, T cell activation and polarization, as well as antibody production. Exploring the mechanisms underlying the roles of ManLAM during mycobacterial infection will aid in improving tuberculosis (TB) prevention, diagnosis and treatment interventions. In this review, we highlight the interaction between ManLAM and receptors, intracellular signalling pathways triggered by ManLAM and its roles in both innate and adaptive immune responses.
Highlights
Tuberculosis (TB), predominately caused by Mycobacterium tuberculosis (M. tb) is a leading cause of death worldwide [1]
The α-mannosyl residues at the non-reducing end of LAM/Mannose-capped lipoarabinomannan (ManLAM) have subsequently been shown to be potent activators of mouse (Vα19) natural killer T (NKT) cells when they are presented by mannose receptor (MR) [48]. These results indicate that the MPI anchor in ManLAM might have the ability to activate NKT cells
In the TB diagnostics field, soluble ManLAM secreted from M. tb and infected cells is an important immunodiagnostic target
Summary
Tuberculosis (TB), predominately caused by Mycobacterium tuberculosis (M. tb) is a leading cause of death worldwide [1]. We highlight the interaction between ManLAM and receptors, intracellular signalling pathways triggered by ManLAM and its role in immunomodulation of both innate and adaptive immunity. Both TLR1/2 and TLR2/6 have been shown to bind with ManLAM and subsequently trigger the MyD88dependent signalling pathway, in which phosphorylation of phosphatidylinositol 3 kinase (PI3 K)/AKT/ Ap-1 and Lys48 (K48)-linked ubiquitination of NFkB are increased (Figure 2) [13].
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