| First Author | Stritesky GL | Year | 2008 |
| Journal | J Immunol | Volume | 181 |
| Issue | 9 | Pages | 5948-55 |
| PubMed ID | 18941183 | Mgi Jnum | J:140746 |
| Mgi Id | MGI:3814497 | Doi | 10.4049/jimmunol.181.9.5948 |
| Citation | Stritesky GL, et al. (2008) IL-23 promotes maintenance but not commitment to the Th17 lineage. J Immunol 181(9):5948-55 |
| abstractText | IL-23 plays a critical role establishing inflammatory immunity and enhancing IL-17 production in vivo. However, an understanding of how it performs those functions has been elusive. In this report, using an IL-17-capture technique, we demonstrate that IL-23 maintains the IL-17-secreting phenotype of purified IL-17(+) cells without affecting cell expansion or survival. IL-23 maintains the Th17 phenotype over multiple rounds of in vitro stimulation most efficiently in conjunction with IL-1beta. However, in contrast to Th1 and Th2 cells, the Th17 phenotype is not stable and when long-term IL-23-stimulated Th17 cultures are exposed to Th1- or Th2-inducing cytokines, the Th17 genetic program is repressed and cells that previously secreted IL-17 assume the cytokine secreting profile of other Th subsets. Thus, while IL-23 can maintain the Th17 phenotype, it does not promote commitment to an IL-17-secreting lineage. |
