Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Hayakawa, S. et al.

Murine fetal resorption and experimental pre-eclampsia are induced by both excessive Th1 and Th2 activation.

It has been proposed that immune responses in mammalian normal pregnancy are Th2-like, thereby protecting the fetus and placenta from being rejected. Administration of exogenous Th1 cytokines into pregnant mice is reported to induce feto-placental resorption. However, the effects of exogenous Th2 cytokines and Th2 directed responses in pregnant animals have not been well studied. In this study, we examined IL-4 and IL-12, which play decisive roles in the development of Th2 and Th1 responses, respectively, in the induction of fetal resorption and development of experimental pre-eclampsia. Transfer of either IL-4 and/or IL-12 stimulated splenocytes from BALB/C virgin female mice into BALB/C pregnant mice mated with either C57BL/6 or BALB/C male mice resulted in fetal resorption and glomerular nephritis associated with hypertension and proteinuria. In mice treated with IL-12 stimulated splenocytes, fatty liver degeneration associated with bile retention was observed. These results indicate that both excessive Th1 and Th2 activation contribute to the development of fetal resorption and pre-eclampsia, but that Th1 is critical to the development of liver degeneration.[1]

References

Murine fetal resorption and experimental pre-eclampsia are induced by both excessive Th1 and Th2 activation. Hayakawa, S., Fujikawa, T., Fukuoka, H., Chisima, F., Karasaki-Suzuki, M., Ohkoshi, E., Ohi, H., Kiyoshi Fujii, T., Tochigi, M., Satoh, K., Shimizu, T., Nishinarita, S., Nemoto, N., Sakurai, I. J. Reprod. Immunol. (2000) [Pubmed]

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