| First Author | Ohteki T | Year | 2006 |
| Journal | J Exp Med | Volume | 203 |
| Issue | 10 | Pages | 2329-38 |
| PubMed ID | 16966429 | Mgi Jnum | J:124624 |
| Mgi Id | MGI:3722042 | Doi | 10.1084/jem.20061297 |
| Citation | Ohteki T, et al. (2006) Essential roles of DC-derived IL-15 as a mediator of inflammatory responses in vivo. J Exp Med 203(10):2329-38 |
| abstractText | Interleukin (IL)-15 is expressed in a variety of inflammatory diseases. However, the contribution of dendritic cell (DC)-derived IL-15 to the development of diseases is uncertain. Using established models of Propionibacterium acnes (P. acnes)- and zymosan-induced liver inflammation, we observed granuloma formation in the livers of wild-type (WT) and RAG-2(-/-) mice but not in those of IL-15(-/-) mice. We demonstrate that this is likely caused by an impaired sequential induction of IL-12, IFN-gamma, and chemokines necessary for monocyte migration. Likewise, lethal endotoxin shock was not induced in P. acnes- and zymosan-primed IL-15(-/-) mice or in WT mice treated with a new IL-15-neutralizing antibody. In both systems, proinflammatory cytokine production was impaired. Surprisingly, neither granuloma formation, lethal endotoxin shock, nor IL-15 production was induced in mice deficient for DCs, and adoptive transfer of WT but not IL-15(-/-) DCs restored the disease development in IL-15(-/-) mice. Collectively, these data indicate the importance of DC-derived IL-15 as a mediator of inflammatory responses in vivo. |
