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The use and misuse of animal analog models of human pregnancy disorders.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Clark, David A.
Description	Author Affiliation: Clark DA ( McMaster University Department of Medicine, Health Sciences Center, Room 3H1E, 1280 Main Street West, Hamilton, Ontario, Canada L8S 4K1)
Abstract	It has been suggested that the differences between placentation in humans and rodents, such as mice, are sufficient to render human pregnancy unique and to justify ignoring data generated using mice. Detailed examination of the placenta-decidua interaction and decidual NK cell composition in humans, and mice, show that the principles are the same. Indeed, the rat placenta is useful in showing an intermediary arrangement between humans and mice. This is consistent with the thesis of Darwin that structures of older species evolve with development of new species to provide a survival advantage. Molecular details may differ between species, but also between individuals given gene polymorphisms. Human data on interaction of HLA-C2 with NK cell KIR receptors has been used to suggest that human pregnancy problems such as recurrent miscarriage, fetal growth retardation, and pre-eclampsia are due to lack of activation of true uterine NK cell (TuNK) functions that promote trophoblast cell growth and invasion which prevents such problems. But when TuNKs bear certain KIR phenotypes, pathology results. It is shown that such mechanisms could only be pertinent in less than one-third of recurrent miscarriage patients. Activated blood-type NK cells that enter the uterus (BuNKs) remain the major effector of pregnancy loss in humans, and this is consistent with data from the mouse. The importance of activated BuNKs in pre-eclampsia and fetal growth retardation merits further investigation as pre-eclampsia and fetal growth restriction are also manifest in the CBAxDBA/2 mouse model where activated NK cells are the initiator of abortions.
File Format	HTM / HTML
ISSN	01650378
Volume Number	103
e-ISSN	18727603
Journal	Journal of Reproductive Immunology
Language	English
Publisher	Elsevier
Publisher Date	2014-06-01
Publisher Place	Ireland
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Immunology Discipline Reproductive Medicine Abortion, Spontaneous Immunology Disease Models, Animal Fetal Growth Retardation Killer Cells, Natural Pre-eclampsia Animals Decidua Embryology Female Hla-c Antigens Humans Mice Mice, Inbred Balb C Mice, Inbred Cba Mice, Inbred Dba Placentation Pregnancy Rats Receptors, Kir Journal Article Review
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology Reproductive Medicine Obstetrics and Gynecology

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Natural killer cells promote immune tolerance by regulating inflammatory TH17 cells at the human maternal-fetal interface.

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Balanced levels of nerve growth factor are required for normal pregnancy progression

Seminal plasma peptides may determine maternal immune response that alters success or failure of pregnancy in the abortion-prone CBAxDBA/2 model.

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HLA reduces killer cell Ig-like receptor expression level and frequency in a humanized mouse model.

The therapeutic potential of the recombinant antigen from Dirofilaria immitis (rDiAg) for immune-mediated pregnancy loss.

The use and misuse of animal analog models of human pregnancy disorders.

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The use and misuse of animal analog models of human pregnancy disorders.