| First Author | Takeda K | Year | 1998 |
| Journal | Immunity | Volume | 8 |
| Issue | 3 | Pages | 383-90 |
| PubMed ID | 9529155 | Mgi Jnum | J:46514 |
| Mgi Id | MGI:1201263 | Doi | 10.1016/s1074-7613(00)80543-9 |
| Citation | Takeda K, et al. (1998) Defective NK cell activity and Th1 response in IL-18-deficient mice. Immunity 8(3):383-90 |
| abstractText | IL-18 is a cytokine that is secreted from activated macrophages and induces IFN gamma production. To investigate the in vivo role of IL-18, we generated IL-18- deficient mice. In Propionibacterium acnes (P. Acnes)- primed IL-18-deficient mice, LPS-induced IFN gamma production was markedly reduced, despite normal IL-12 induction. Natural killer cell activity was significantly impaired. Th1 cell response after injection of P. Acnes or Mycobacterium bovis (bacillus Calmette-Guerin [BCG]) was significantly reduced. Similar results were observed in IL- 12-deficient mice. Interestingly, Th1 response was induced after BCG infection in IL-12-deficient mice. We therefore generated mice lacking both IL-18 and IL-12. In these mice, NK activity and Th1 response were further impaired. This demonstrates the important role of both IL-18 and IL- 12 in NK activity, as well as in in vivo Th1 response. |
