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• W4313377541 endingPage "102294" @default.
• W4313377541 startingPage "102294" @default.
• W4313377541 abstract "Mycobacteria often cause chronic infection. To establish persistence in the host, mycobacteria need to evade host immune responses. However, the molecular mechanisms underlying the evasion strategy are not fully understood. Here, we demonstrate that mycobacterial cell wall lipids trigger an inhibitory receptor to suppress host immune responses. Mycolic acids are major cell wall components and are essential for survival of mycobacteria. By screening inhibitory receptors that react with mycobacterial lipids, we found that mycolic acids from various mycobacterial species bind to mouse Clec12A, and more potently to human Clec12A. Clec12A is a conserved inhibitory C-type lectin receptor containing immunoreceptor tyrosine-based inhibitory motif (ITIM). Innate immune responses, such as MCP-1 production, and PPD-specific recall T cell responses were augmented in Clec12A-deficient mice after infection. In contrast, human Clec12A transgenic mice were susceptible to infection with M. tuberculosis. These results suggest that mycobacteria dampen host immune responses by hijacking an inhibitory host receptor through their specific and essential lipids, mycolic acids. The blockade of this interaction might provide a therapeutic option for the treatment or prevention of mycobacterial infection." @default.
• W4313377541 created "2023-01-06" @default.
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• W4313377541 date "2023-01-01" @default.
• W4313377541 modified "2023-10-14" @default.
• W4313377541 title "Mycobacterial mycolic acids trigger inhibitory receptor Clec12A to suppress host immune responses" @default.
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• W4313377541 doi "https://doi.org/10.1016/j.tube.2022.102294" @default.
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• W4313377541 hasPublicationYear "2023" @default.
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