期刊
JOURNAL OF INFECTIOUS DISEASES
卷 198, 期 9, 页码 1284-1291出版社
OXFORD UNIV PRESS INC
DOI: 10.1086/592048
关键词
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资金
- Flanders-South African Research Cooperation
- Medical Research Council
- National Research Foundation
- National Health and Laboratory Services, South Africa
- Fonds voor Wetenschappelijk Onderzoek-Vlaanderen
To determine the immunological role played by interleukin (IL)-12 family members in Trypanosoma congolense infection, IL-12p35(-/-), IL-12p40(-/-), and IL-12p35(/-/-)p40(-/-) mice were used. While the latter 2 strains lack all IL-12 homologues, IL-12p35m(-/-) ice still produce IL-12p80 homodimers and IL-23. Compared with wild-type mice, all infected IL-12-deficient mouse strains showed prolonged survival, whereas parasitemia levels were unaltered. Interferon (IFN)-gamma production in IL-12-deficient mice was strikingly reduced during the acute and chronic stages of infection, coinciding with significantly reduced chronic-stage hepatocellular damage, as demonstrated by histological analysis and plasma aspartate transaminase measurements. In contrast, IL-10 production was not affected by the absence of IL-12. Taken together, these results show that, during T. congolense infection, the absence of IL-12, but not the IL-12p80 homodimer or IL-23, leads to a reduction in IFN-gamma production, which reduces hepatic pathology and improves host survival in conjunction with IL-10 without negatively affecting parasitemia control.
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