Send to

Choose Destination
See comment in PubMed Commons below
J Reprod Immunol. 2009 Dec;83(1-2):85-94. doi: 10.1016/j.jri.2009.07.011. Epub 2009 Oct 29.

The impact of dendritic cells on angiogenic responses at the fetal-maternal interface.

Author information

  • 1CharitĂ©, Department of Internal Medicine and Dermatology, Medicine University of Berlin, Berlin, Germany.


The success of mammalian pregnancy is highly dependent on the establishment of an adequate blood supply to support the metabolic demands of the growing embryo and fetus. New blood vessels develop from pre-existing vessels in a multi-step process called angiogenesis, which is tightly regulated in time and space and has proven to be crucial in several physiological situations such as wound healing, follicular development and cyclic endometrial growth. As in other tissues, the regulation of angiogenic responses in the decidua depends on a delicate balance between stimulatory and inhibitory signals. In particular, trophoblasts and decidual NK cells are well-recognized components of the uterine signaling network with a proven ability to produce growth factors and cytokines that modulate endothelial cell responsiveness during pregnancy. In mice and humans, dendritic cells are also considered an important regulatory component during pregnancy, mainly due to their role in the establishment of maternal immunologic tolerance. However, the recent finding that dendritic cell subsets can promote angiogenesis in a variety of physiopathological settings suggests that regulatory functions of these cells may go beyond the promotion of maternal tolerance, having impact on other processes such as decidualization and placentation and the vascular changes associated to them. Current evidence on dendritic cell-derived angiogenic signals and their potential implications in vascular development during gestation are reviewed and discussed herein.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk