Interleukin-12p70 deficiency increases survival and diminishes pathology in Trypanosoma congolense infection.

TitleInterleukin-12p70 deficiency increases survival and diminishes pathology in Trypanosoma congolense infection.
Publication TypeJournal Article
Year of Publication2008
AuthorsBarkhuizen, M., S. Magez, B. Ryffel, and F. Brombacher
JournalJ Infect Dis
Date Published2008 Nov 1
KeywordsAnimals, Antibodies, Protozoan, Immunity, Innate, Immunoglobulin G, Interferon-gamma, Interleukin-12, Interleukin-23, Liver, Mice, Mice, Knockout, Parasitemia, Protein Subunits, Time Factors, Trypanosoma congolense, Trypanosomiasis, African

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-12p35(-/-) mice 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.

Alternate JournalJ. Infect. Dis.
PubMed ID18816189