| First Author | del Fresno C | Year | 2013 |
| Journal | Immunity | Volume | 38 |
| Issue | 6 | Pages | 1176-86 |
| PubMed ID | 23770228 | Mgi Jnum | J:207582 |
| Mgi Id | MGI:5559139 | Doi | 10.1016/j.immuni.2013.05.010 |
| Citation | del Fresno C, et al. (2013) Interferon-beta production via Dectin-1-Syk-IRF5 signaling in dendritic cells is crucial for immunity to C. albicans. Immunity 38(6):1176-86 |
| abstractText | Type I interferon (IFN) is crucial during infection through its antiviral properties and by coordinating the immunocompetent cells involved in antiviral or antibacterial immunity. Type I IFN (IFN-alpha and IFN-beta) is produced after virus or bacteria recognition by cytosolic receptors or membrane-bound TLR receptors following the activation of the transcription factors IRF3 or IRF7. IFN-beta production after fungal infection was recently reported, although the underlying mechanism remains controversial. Here we describe that IFN-beta production by dendritic cells (DCs) induced by Candida albicans is largely dependent on Dectin-1- and Dectin-2-mediated signaling. Dectin-1-induced IFN-beta production required the tyrosine kinase Syk and the transcription factor IRF5. Type I IFN receptor-deficient mice had a lower survival after C. albicans infection, paralleled by defective renal neutrophil infiltration. IFN-beta production by renal infiltrating leukocytes was severely reduced in C. albicans-infected mice with Syk-deficient DCs. These data indicate that Dectin-induced IFN-beta production by renal DCs is crucial for defense against C. albicans infection. |
