Type-I interferon secretion in the acute phase promotes Cryptococcus neoformans infection-induced Th17 cell polarization in vitro.

Cryptococcosis is a potentially fatal fungal disease commonly identified in patients with acquired immunodeficiency syndrome. Cryptococcus infection induces strong pro-inflammatory cytokine secretion, i.e. type-I interferon (IFN-I) via the Toll-like receptor signaling pathway. However, innate immune responses are insufficient in host defense against fungi infection and the clearance of Cryptococcus is dependent on the T helper (Th)17 cell-mediated mucosal immune response. In this study, IFN-I was identified as the early response cytokine to Cryptococcus neoformans infection via quantitative PCR (qPCR) and IFN-I was demonstrated to be crucial for interleukin (IL)-17A secretion in T cells, but not in innate immune cells. In addition, blockade of IFN-I reduced the protein expression levels of IL-22 and IL-23 in Th17 cells in vitro. These results suggest additional functions of IFN-I in immune regulation, which may be pivotal for the development of clinical immune therapy.