| First Author | Kleinschek MA | Year | 2010 |
| Journal | Int Immunol | Volume | 22 |
| Issue | 2 | Pages | 81-90 |
| PubMed ID | 19951959 | Mgi Jnum | J:157781 |
| Mgi Id | MGI:4436964 | Doi | 10.1093/intimm/dxp117 |
| Citation | Kleinschek MA, et al. (2010) Administration of IL-23 engages innate and adaptive immune mechanisms during fungal infection. Int Immunol 22(2):81-90 |
| abstractText | IL-23 is a key cytokine in promotion of chronic inflammation. Here, we address if its pro-inflammatory potential can be harnessed to protect against chronic cryptococcosis. Mice were infected with Cryptococcus neoformans and treated with recombinant IL-23. Administration of IL-23 led to prolonged survival and reduced fungal burden but was inferior to IL-12 treatment. Independent of endogenous IL-23/IL-12, IL-23 treatment induced an altered cytokine profile accompanied by marked changes in composition of the inflammatory infiltrate characterized by T cell and dendritic cell recruitment. Although IL-23 induced hallmarks of the T(h)17 pathway, also non-T cells produced IL-17A and IL-22. IL-23 treatment of T-cell-deficient mice resulted in increased IL-17A and IL-22 production and modulation of the cellular response at the site of infection with elevated expression of CD86 on macrophages. Our data show that IL-23 treatment induces innate and adaptive tissue inflammation with limited impact on resistance to chronic cryptococcosis. |
