| First Author | Curtis MM | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 1 | Pages | 381-7 |
| PubMed ID | 19542449 | Mgi Jnum | J:149971 |
| Mgi Id | MGI:3849496 | Doi | 10.4049/jimmunol.0900939 |
| Citation | Curtis MM, et al. (2009) IL-23 promotes the production of IL-17 by antigen-specific CD8 T cells in the absence of IL-12 and type-I interferons. J Immunol 183(1):381-7 |
| abstractText | In contrast to CD4 T cells, CD8 T cells inherently differentiate into IFN-gamma-producing effectors. Accordingly, while generation of IFN-gamma-producing Th1 CD4 T cells was profoundly impaired in mice deficient for both type-I IFN and IL-12 signaling in response to infection with Listeria monocytogenes, generation of Ag-specific, IFN-gamma-producing CD8 T cells was unimpaired. However, a fraction of these CD8 T cells also produced IL-17 in an IL-23-dependent manner. Furthermore, the addition of IL-23 in vitro was sufficient for some naive CD8 T cells to differentiate into IFN-gamma/IL-17 dual-producing cells and was associated with increased expression of ROR-gammat and ROR-alpha. Addition of IL-6 and TGF-beta to IL-23 further augmented ROR-gammat and ROR-alpha expression and suppressed Eomes expression, thereby enhancing IL-17 production by CD8 T cells. A loss of cytotoxic function accompanied the production of IL-17, as the addition of IL-6 and TGF-beta resulted in a marked reduction of granzyme B and perforin expression. Thus, CD8 T cells retain sufficient plasticity to respond to environmental cues and can acquire additional effector functions in response to their environmental context. |
