| First Author | Diefenbach A | Year | 1999 |
| Journal | Science | Volume | 284 |
| Issue | 5416 | Pages | 951-5 |
| PubMed ID | 10320373 | Mgi Jnum | J:54604 |
| Mgi Id | MGI:1336535 | Doi | 10.1126/science.284.5416.951 |
| Citation | Diefenbach A, et al. (1999) Requirement for type 2 NO synthase for IL-12 signaling in innate immunity [published erratum appears in Science 1999 Jun 11;284(5421):1776]. Science 284(5416):951-5 |
| abstractText | Interleukin-12 (IL-12) and type 2 NO synthase (NOS2) are crucial for defense against bacterial and parasitic pathogens, but their relationship in innate immunity is unknown. In the absence of NOS2 activity, IL-12 was unable to prevent spreading of Leishmania parasites, did not stimulate natural killer (NK) cells for cytotoxicity or interferon-gamma (IFN-gamma) release, and failed to activate Tyk2 kinase and to tyrosine phosphorylate Stat4 (the central signal transducer of IL-12) in NK cells. Activation of Tyk2 in NK cells by IFN-alpha/beta also required NOS2. Thus, NOS2-derived NO is a prerequisite for cytokine signaling and function in innate immunity. |
