The investigators found that signaling through Dectin-1, a cell surface receptor specialized for the recognition of fungi, alters the immune cytokine pattern resulting in a qualitatively different inflammatory response. Working with mice with a genetic deficiency in Dectin-1, the authors discovered that signaling through this receptor inhibits the cytokines IL-12 and interferon gamma. As these cytokines inhibit IL-17 induction, signaling through Dectin-1 results in a commensurate increase in IL-17, a cytokine known to mediate protective effects against fungal infection in humans. The current work by Rivera and colleagues lays the theoretical groundwork for efforts to study and manipulate the immune response to fungi by controlling signaling through the receptors that initially recognize fungal pathogens.
This study was supported by grants from the National Cancer Institute (NCI) and the National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health. Authors, in addition to Rivera, were Tobias M. Hohl of Fred Hutchinson Cancer Research Center; Eric G. Pamer, Nichole Collins, Ingrid Leiner and Jesse W. Coward of Memorial Sloan-Kettering Cancer Center (MSKCC); Alena Gallegos of NIAID; Shinobu Saijo and Yoichiro Iwakura of the University of Tokyo.
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