Figure 1

Figure 1. Model of Fungal iNKT Activation. From: iNKTs Foil Fungi.

In (1), fungi expose cell wall β-(1,3) glucan following morphological transitions (e.g., conidial swelling [Aspergillus fumigatus]), cell division (e.g., bud or birth scars [Candida albicans]), or disruption of the external α-glucan layer (Histoplasma capsulatum). In (2), β-(1,3) glucan ligation at the cell surface or within phagosomes induces dectin-1 signaling, which, in concert with collaborative Toll-like receptor signaling, leads to DC activation. In (3), DC-derived IL-12 is a key element for iNKT activation together with CD1d-dependent TCR interactions, although A. fumigatus-derived lipids do not appear to contribute to iNKT activation, consistent with a role for endogenous lipid antigen (shown in yellow) presentation to the iNKT TCR. In (4), rapid release of effector cytokines such as IFN-γ by iNKT cells follows activation. How iNKT activation mediates enhanced fungal clearance in vivo remains an important unresolved question.

Martin Prlic, et al. Cell Host Microbe. ;10(5):421-422.

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