IL-22 in antifungal immunity.
Deciphering cellular and molecular mechanisms that maintain host immune homeostasis with fungi and the breakdown of this homeostatic tolerance during fungal infections disease is a challenge in medical mycology. In fact, the virulence of fungi may be determined by the interaction between fungi and the host immune status and its classification as a commensal microorganism or a pathogen may shift depending on the balance. In addition to the central role of the IL-12/IFN-γ-dependent Th1 responses in cell-mediated immune protection against fungi, Th17 cells provide protection and inflammation at mucosal surfaces, and Tregs fine-tune immune responses to prevent damage to the host. Recent evidence indicates that IL-22-producing cells, employing primitive antifungal effector mechanisms, contribute to antifungal resistance at mucosal surfaces under conditions of defective adaptive immunity. The fact that IL-22 production is driven by commensals points to the need of an integrated, systems biology approach to improve our understanding of the inherent and intimate mechanisms underlying multilevel host-fungus interactions.
Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Perugia, Italy.
Teresa
T
Zelante
Rossana
R
Iannitti
Antonella
A
De Luca
Luigina
L
Romani
D000818:Animals; D006801:Humans; D018928:Immunity, Mucosal / Q000276:immunology; D007378:Interleukins / Q000276:immunology*; D054892:Metagenome / Q000276:immunology; D009181:Mycoses / Q000276:immunology*; D000097043:Interleukin-22
D007378:Interleukins; D000097043:Interleukin-22