| First Author | Duthie MS | Year | 2006 |
| Journal | Immunology | Volume | 119 |
| Issue | 3 | Pages | 355-61 |
| PubMed ID | 16879622 | Mgi Jnum | J:118525 |
| Mgi Id | MGI:3699738 | Doi | 10.1111/j.1365-2567.2006.02439.x |
| Citation | Duthie MS, et al. (2006) During acute Trypanosoma cruzi infection highly susceptible mice deficient in natural killer cells are protected by a single alpha-galactosylceramide treatment. Immunology 119(3):355-61 |
| abstractText | The protective immune response against Trypanosoma cruzi is improved by treatment with the natural killer (NK) T-cell glycolipid antigen alpha-galactosylceramide (alpha-GalCer). A single alpha-GalCer treatment of mice before T. cruzi infection decreases parasitaemia and prolongs survival. This protection is dependent on CD1d-restricted NKT cells and interferon-gamma (IFN-gamma) suggesting that alpha-GalCer-activated NKT cells produce IFN-gamma, which stimulates the cells of the innate and adaptive immune responses to provide protection. To learn which cells provide protection we investigate here alpha-GalCer treatment of mice deficient in different immune cells. Surprisingly, although NK cells provide protection against T. cruzi, and are a major source of IFN-gamma following alpha-GalCer treatment, NK cells are not required for the alpha-GalCer-induced protection. The alpha-GalCer treatment of NK-cell-depleted mice controlled parasitaemia and prevented death. In contrast, phagocytes, helper T cells and cytotoxic T cells are required. Furthermore, alpha-GalCer treatment of MHC II(-/-) or CD8alpha(-/-) mice exacerbated the infection, demonstrating that alpha-GalCer treatment induces some responses that favour the parasite. In summary alpha-GalCer protection against T. cruzi required multiple cellular responses, but not the response of NK cells. These results provide useful information because alpha-GalCer is being developed as therapy for infections, autoimmune diseases, allergy and cancers. |
