Journal
AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
Volume 63, Issue 6, Pages 534-543Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1600-0897.2010.00831.x
Keywords
HLA-C; immunoregulation; indoleamine 2; 3-dioxygenase; NK cells; placentation; regulatory T cells; systemic inflammatory response
Categories
Funding
- Wellcome Trust [GR079862MA]
- Department of Health's NIHR Biomedical Research Centres
Ask authors/readers for more resources
Pre-eclampsia develops in stages, only the last being the clinical illness. This is generated by a non-specific, systemic (vascular), inflammatory response, secondary to placental oxidative stress and not by reactivity to fetal alloantigens. However, maternal adaptation to fetal (paternal alloantigens) is crucial in the earlier stages. A pre-conceptual phase involves maternal tolerization to paternal antigens by seminal plasma. After conception, regulatory T cells, interacting with indoleamine 2,3-dioxygenase, together with decidual NK cell recognition of fetal HLA-C on extravillous trophoblast may facilitate placental growth by immunoregulation. Complete failure of this mechanism would cause miscarriage, while partial failure would cause poor placentation and dysfunctional uteroplacental perfusion. The first pregnancy preponderance and partner specificity of pre-eclampsia can be explained by this model. For the first time, the pathogenesis of pre-eclampsia can be related to defined immune mechanisms that are appropriate to the fetomaternal frontier. Now, the challenge is to prove the detail.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available