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A pregnant pause for unexpected interactions

Approximately 1-3% of all couples experience recurrent pregnancy loss, and about 5070% of all conceptions fail. The underlying molecular mechanisms causing these heartbreaking conditions, however, remain unknown. Many cases of pregnancy loss are known to due to damage to the fetus through genetic, anatomic, endocrine, or Infectious means.

When such causes are ruled out, the other source is thought to be caused by a maternal immune response. Most of the research in this arena has focused on identifying reactions at the maternal-fetal interface in the placenta. Adrian Erlebacher and colleagues, from Harvard School of Public Health, have now, however, identified new means by which maternal immune activation can lead to pregnancy failure. Here, the authors provide a mouse model of early pregnancy loss and present data that unexpectedly links the reproductive hormone secretion system to the immune system.

The mouse model shows that when a specific immune cell receptor called CD40 is activated early in pregnancy the resulting inflammatory response caused embryo resorption. The researchers traced the molecular mechanisms underlying this process, and found that the loss of the embryo was not due to fetal damage or activity at the fetal-maternal interface, but rather because the inflammatory response ultimately caused a decrease in progesterone, the hormone responsible for preparing the body for pregnancy and maintaining it until birth.

These data make it clear that the immune system, by interfering with the reproductive hormones, may contribute to human infertility, especially in cases of recurrent pregnancy loss. Further the finding that there is a link between the immune system and the reproductive hormone secretion may provide a new means of therapy for women who suffer such repeated and early pregnancy loss by targeting the mediators of such inflammatory responses.


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Contact: Laurie Goodman
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
1-Jul-2004


Page: 1

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