| First Author | Jankovic D | Year | 2002 |
| Journal | Immunity | Volume | 16 |
| Issue | 3 | Pages | 429-39 |
| PubMed ID | 11911827 | Mgi Jnum | J:113516 |
| Mgi Id | MGI:3686912 | Doi | 10.1016/s1074-7613(02)00278-9 |
| Citation | Jankovic D, et al. (2002) In the absence of IL-12, CD4(+) T cell responses to intracellular pathogens fail to default to a Th2 pattern and are host protective in an IL-10(-/-) setting. Immunity 16(3):429-39 |
| abstractText | IL-12-deficient mice exposed to nonlethal infections with intracellular pathogens or repeatedly immunized with a pathogen extract developed lowered but nevertheless substantial numbers of IFN-gamma(+) CD4(+) T cells compared to those observed in wild-type animals. Moreover, the CD4(+) responses in these knockout animals failed to default to a Th2 pattern. The protective efficacy of the Th1 cells developing in an IL-12-deficient setting was found to be limited by IL-10 since mice doubly deficient in IL-10 and IL-12 survived, while animals deficient in IL-12 alone succumbed to pathogen challenge. In contrast to IL-12 knockout mice, MyD88-deficient animals exposed to a Th1 microbial stimulus developed a pure Th2 response, arguing that this signaling element plays a more critical function than IL-12 in determining pathogen-induced CD4 polarization. |
