| First Author | Patin EC | Year | 2016 |
| Journal | J Immunol | Volume | 197 |
| Issue | 1 | Pages | 208-21 |
| PubMed ID | 27259855 | Mgi Jnum | J:263060 |
| Mgi Id | MGI:6120585 | Doi | 10.4049/jimmunol.1501204 |
| Citation | Patin EC, et al. (2016) IL-27 Induced by Select Candida spp. via TLR7/NOD2 Signaling and IFN-beta Production Inhibits Fungal Clearance. J Immunol 197(1):208-21 |
| abstractText | Candida spp. elicit cytokine production downstream of various pathogen recognition receptors, including C-type lectin-like receptors, TLRs, and nucleotide oligomerization domain (NOD)-like receptors. IL-12 family members IL-12p70 and IL-23 are important for host immunity against Candida spp. In this article, we show that IL-27, another IL-12 family member, is produced by myeloid cells in response to selected Candida spp. We demonstrate a novel mechanism for Candida parapsilosis-mediated induction of IL-27 in a TLR7-, MyD88-, and NOD2-dependent manner. Our data revealed that IFN-beta is induced by C. parapsilosis, which in turn signals through the IFN-alpha/beta receptor and STAT1/2 to induce IL-27. Moreover, IL-27R (WSX-1)-deficient mice systemically infected with C. parapsilosis displayed enhanced pathogen clearance compared with wild-type mice. This was associated with increased levels of proinflammatory cytokines in the serum and increased IFN-gamma and IL-17 responses in the spleens of IL-27R-deficient mice. Thus, our data define a novel link between C. parapsilosis, TLR7, NOD2, IFN-beta, and IL-27, and we have identified an important role for IL-27 in the immune response against C. parapsilosis Overall, these findings demonstrate an important mechanism for the suppression of protective immune responses during infection with C. parapsilosis, which has potential relevance for infections with other fungal pathogens. |
