| First Author | Monteforte GM | Year | 2000 |
| Journal | J Immunol | Volume | 164 |
| Issue | 11 | Pages | 5890-3 |
| PubMed ID | 10820270 | Mgi Jnum | J:62240 |
| Mgi Id | MGI:1858628 | Doi | 10.4049/jimmunol.164.11.5890 |
| Citation | Monteforte GM, et al. (2000) Genetically resistant mice lacking IL-18 gene develop Th1 response and control cutaneous Leishmania major infection. J Immunol 164(11):5890-3 |
| abstractText | IL-18 has been shown to play a critical role in the development of a Th1 response and immunity against intracellular pathogens. To determine the role of IL-18 in the development of protective immunity against Leishmania major, we have analyzed the course of cutaneous L. major in IL-18-deficient C57BL/6 mice (IL-18-/-) compared with similarly infected wild-type mice (IL-18+/+). After L. major infection, IL-18-/- mice may develop larger lesions during early phase of infection but eventually will resolve them as efficiently as IL-18+/+ mice. By 2 wk after infection, although Ag-stimulated lymph node cells from L. major-infected IL-18+/+ and IL-18-/- mice produced similar levels of IFN-gamma, those from IL-18-/- mice produced significantly more IL-12 and IL-4. By 10 wk after infection, both IL-18+/+ and IL-18-/- mice had resolved L. major infection. At this time, lymph node cells from both IL-18+/+ and IL-18-/- mice produced IL-12 and IFN-gamma but no IL-4. Furthermore, administration of anti-IFN-gamma Abs to IL-18-/- mice rendered them susceptible to L. major. These results indicate that despite the role IL-18 may play in early control of cutaneous L. major lesion growth, this cytokine is not critical for development of protective Th1 response and resolution of L. major infection. |
