| First Author | Lewkowich IP | Year | 2002 |
| Journal | Eur J Immunol | Volume | 32 |
| Issue | 12 | Pages | 3536-45 |
| PubMed ID | 12442336 | Mgi Jnum | J:80855 |
| Mgi Id | MGI:2447286 | Doi | 10.1002/1521-4141(200212)32:12<3536::AID-IMMU3536>3.0.CO;2-U |
| Citation | Lewkowich IP, et al. (2002) Endogenous IFN-gamma and IL-18 production directly limit induction of type 2 immunity in vivo. Eur J Immunol 32(12):3536-45 |
| abstractText | Allergic diseases are associated with excessive type 2 immunity, yet the endogenous controls - if any - responsible for limiting induction of such responses remain unclear. Using IL-12-deficient mice, we recently showed that endogenous IL-12 is not essential for preventing development of allergic responses. Here, we examine the roles of endogenous IFN-gamma and IL-18 production in limiting the occurrence and severity of type 2 immunity. Lack of endogenous IFN-gamma synthesis results in significantly higher type 2 cytokine (IL-4, IL-5, IL-10 and IL-13) and chemokine (TARC) production following exogenous antigen exposure. Thus, IFN-gamma, but not IL-12, is a key negative regulator of the type 2 immune response. IL-18, in addition to its established role as an inducer of IFN-gamma, also negatively regulates CD4(+) T cell-derived IL-4 synthesis via an IFN-gamma-independent mechanism, thereby further limiting the development of type 2 immune responses. Together, theseresults identify endogenous IFN-gamma and IL-18 as potent, independent, negative regulators of the development of type 2 immunity to ubiquitous environmental antigens. |
