期刊
INFECTION AND IMMUNITY
卷 72, 期 2, 页码 988-995出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.72.2.988-995.2004
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资金
- NIAID NIH HHS [AI43003, R01 AI043003, R56 AI043003] Funding Source: Medline
During Leishmania major infection in mice, gamma interferon (IFN-gamma) plays an essential role in controlling parasite growth and disease progression. In studies designed to ascertain the role of IFN-gamma in Leishmania amazonensis infection, we were surprised to find that IFN-gamma could promote L. amazonensis amastigote replication in macrophages (MPhis), although it activated MPhis to kill promastigotes. The replication-promoting effect of IFN-gamma on amastigotes was independent of the source and genetic background of MPhis, was apparently not affected by surface opsonization of amastigotes, was not mediated by interleukin-10 or transforming growth factor beta, and was observed at different temperatures. Consistent with the different fates of promastigotes and amastigotes in IFN-gamma-stimulated MPhis L. amazonensis-specific Th1 transfer helped recipient mice control L. amazonensis infection established by promastigotes but not L. amazonensis infection established by amastigotes. On the other hand, IFN-gamma could stimulate MPhis to limit amastigote replication when it was coupled with lipopolysaccharides but not when it was coupled with tumor necrosis factor alpha. Thus, IFN-gamma may play a bidirectional role at the level of parasite-MPhi interactions; when it is optimally coupled with other factors, it has a protective effect against infection, and in the absence of such synergy it promotes amastigote growth. These results reveal a quite unexpected aspect of the L. amazonensis parasite and have important implications for understanding the pathogenesis of the disease and for developing vaccines and immunotherapies.
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