Clec7a-mediated regulation of Killer-like Lectin Receptor expression controls T cell immunity
Dambuza, I. M.; Salazar, F.; Sey, E. A.; Kastora, S. L.; Rodrigues, C.; Phillips-Brookes, A.; Harvey, J.; Drummond, R. A.; Rush, J.; Yuecel, R.; Saijo, S.; Willment, J. A.; Kaplan, D. H.; LeibundGut-Landmann, S.; Brown, G. D.
Show abstract
Clec7a is a C-type lectin receptor (CLR) originally defined for its non-redundant role in anti-fungal immunity. Subsequent work has broadened this view, implicating Clec7a in host defense against diverse pathogens and in the pathogenesis of cancer, autoimmunity, neuroinflammation, and developmental disorders. How a single innate receptor orchestrates such wide-ranging outcomes remains unresolved. We previously demonstrated that dendritic cell (DC)-expressed Clec7a is required for protective anti-fungal immunity in the gastrointestinal tract through regulation of fungus-specific CD4 T cell responses. Here, we show that Clec7a controls the expression of multiple C-type lectins in DCs, including a cluster of killer lectin-like receptors (KLRs). Notably, we reveal that these KLRs directly regulate DC function and control CD4 T cell responses. These findings define a novel Clec7a-KLR axis that integrates innate and adaptive immunity, highlighting a regulatory pathway with broad relevance for immune homeostasis, inflammation, and host defense.
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