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Interleukin-17 (IL-17) producing T helper cells (T H -17) comprise a newly recognized T cell subset with an emerging role in adaptive immunity to a variety of fungi. Whether different airborne fungi trigger a common signaling pathway for T H -17 induction, and whether this ability is related to the inherent pathogenic behavior of each fungus is currently unknown. Here we show that, as opposed to primary pathogenic fungi ( Histoplasma capsulatum ), opportunistic fungal pathogens ( Aspergillus  and  Rhizopus ) trigger a common innate sensing pathway in human dendritic cells (DCs) that results in robust production of IL-23 and drives T H -17 responses. This response requires activation of  dectin-1  by the fungal cell wall polysaccharide b-glucan that is selectively exposed during the invasive growth of opportunistic fungi. Notably, unmasking of b-glucan in the cell wall of a mutant of  Histoplasma  not only abrogates the pathogenicity of this fungus, but also triggers the induction of IL-23 producing DCs. Thus, b-glucan exposure in the fungal cell wall is essential for the induction of IL-23/T H -17 axis and may represent a key factor that regulates protective immunity to opportunistic but not pathogenic fungi.

Generation of IL-23 Producing Dendritic Cells (DCs) by Airborne Fungi Regulates Fungal Pathogenicity via the Induction of TH-17 Responses