C-Type Lectin Receptor Mediated Immunity in Mycobacterial Infections
Summary
C-type lectin receptors (CLRs) represent a family of pattern recognition receptors expressed predominantly on myeloid cells, including macrophages, dendritic cells and neutrophils. These receptors detect distinct carbohydrate and glycolipid motifs within the mycobacterial cell envelope, most notably trehalose-6,6′-dimycolate (cord factor) and related lipids. Ligand binding triggers intracellular signalling cascades through phosphorylation of spleen tyrosine kinase (Syk) and assembly of the CARD9–BCL10–MALT1 complex, culminating in activation of NF-κB and MAP kinases. The resulting transcriptional programme drives cytokine secretion, phagocytosis, reactive oxygen species production and granuloma formation. CLR engagement also shapes adaptive immunity by polarising T helper cell responses, particularly promoting Th1 and Th17 subsets that are critical for containment of Mycobacterium tuberculosis. Genetic variation in CLR-encoding genes and modulation by Th2 cytokines such as interleukin 4 can attenuate receptor expression or function, influencing susceptibility to tuberculosis. In parallel, synthetic and natural CLR ligands have been harnessed as adjuvants to enhance vaccine-induced protection. Together, these insights underscore the global significance of CLR-mediated recognition in balancing protective immunity against mycobacterial pathogens and inform rational design of novel immunoprophylactic strategies.
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C-Type Lectin Receptor Mediated Immunity in Mycobacterial Infections publication trend
The graph below shows the total number of articles in c-type lectin receptor mediated immunity in mycobacterial infections across all publications each year (not limited to Nature Index journals).
Technical terms
C-type lectin receptor (CLR): A pattern recognition receptor that binds carbohydrate or glycolipid motifs, initiating innate immune signalling.
Mincle: Macrophage inducible C-type lectin that recognises mycobacterial trehalose dimycolate and activates Syk-CARD9 signalling.
Dectin-1: A CLR that binds β-glucans and certain mycobacterial ligands, promoting phagocytosis and reactive oxygen species generation.
Trehalose dimycolate (TDM): A mycobacterial cell-wall glycolipid (cord factor) that serves as a potent CLR ligand and adjuvant.
Syk–CARD9 pathway: Intracellular kinase cascade linking CLR engagement to NF-κB activation and pro-inflammatory gene expression.
Th1 and Th17 responses: Subsets of CD4+ T helper cells characterised by interferon-γ (Th1) or interleukin-17 (Th17) production, essential for immunity to intracellular pathogens.
References
- Variants of human DECTIN-1 rs16910526 are linked to differential reactive oxygen species production and susceptibility to tuberculosis. Journal of Biomedical Science (2024).
- IL-4 and helminth infection downregulate MINCLE-dependent macrophage response to mycobacteria and Th17 adjuvanticity. eLife (2023).
- Vaccination with Mincle agonist UM-1098 and mycobacterial antigens induces protective Th1 and Th17 responses. npj Vaccines (2024).
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