| Autor: |
Neighbors M; Department of Immunology, DNAX Research Institute of Molecular and Cellular Biology, Incorporated, Palo Alto, CA 94304, USA. margaret.neighbors@dnax.org, Xu X, Barrat FJ, Ruuls SR, Churakova T, Debets R, Bazan JF, Kastelein RA, Abrams JS, O'Garra A |
| Jazyk: |
angličtina |
| Zdroj: |
The Journal of experimental medicine [J Exp Med] 2001 Aug 06; Vol. 194 (3), pp. 343-54. |
| DOI: |
10.1084/jem.194.3.343 |
| Abstrakt: |
The stimulation of interferon (IFN)-gamma by interleukin (IL)-12 has been shown to provide protection from intracellular pathogens such as Listeria monocytogenes. Tumor necrosis factor (TNF) is also a major player in the resolution of Listeria infections and is suggested to have more global effects than can be explained by the induction of IFN-gamma alone. Since IL-18 synergizes with IL-12 to induce IFN-gamma production by natural killer and T helper (Th)1 cells, we determined its role in responses to Listeria. IL-18 appeared to be even more potent than either IL-12 or IFN-gamma for protection against this pathogen and IL-18 enhanced bacterial clearance in the complete absence of IFN-gamma. Indeed IL-18 was comparable to TNF in its ability to resolve the infection and showed a lowered protective capacity in the absence of TNF. Moreover, IL-18 induced macrophages to secrete both TNF and nitric oxide after a Listeria infection. IL-18 was also essential for optimal IFN-gamma production by antigen-specific T cells. Therefore, IL-18 operates via its effects on both the innate immune response, including macrophages, as well as on Th1 cells, to protect against Listeria. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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