REVIEW ARTICLE: Immunology of Pre-Eclampsia
Version of Record online: 23 MAR 2010
© 2010 John Wiley & Sons A/S
American Journal of Reproductive Immunology
Volume 63, Issue 6, pages 534–543, June 2010
How to Cite
Redman, C. W. G. and Sargent, I. L. (2010), REVIEW ARTICLE: Immunology of Pre-Eclampsia. American Journal of Reproductive Immunology, 63: 534–543. doi: 10.1111/j.1600-0897.2010.00831.x
- Issue online: 10 MAY 2010
- Version of Record online: 23 MAR 2010
- Submitted February 1, 2010; accepted February 1, 2010.
- indoleamine 2,3-dioxygenase;
- NK cells;
- regulatory T cells;
- systemic inflammatory response
Citation Redman CWG, Sargent IL. Immunology of Pre-eclampsia. Am J Reprod Immunol 2010
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.