NK IN PREGNANCY

Impact of Natural Killer Cells on Fetal and Placental Development

Coordinatore	THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE    more  Organization address address: The Old Schools, Trinity Lane city: CAMBRIDGE postcode: CB2 1TN contact info Titolo: Ms. Nome: Renata Cognome: Schaeffer Email: send email Telefono: +44 1223 333543 Fax: +44 1223 332988
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	209˙033 €
EC contributo	209˙033 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2011-IEF
Funding Scheme	MC-IEF
Anno di inizio	2013
Periodo (anno-mese-giorno)	2013-05-01   -   2015-04-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE  Organization address address: The Old Schools, Trinity Lane city: CAMBRIDGE postcode: CB2 1TN contact info Titolo: Ms. Nome: Renata Cognome: Schaeffer Email: send email Telefono: +44 1223 333543 Fax: +44 1223 332988	UK (CAMBRIDGE)	coordinator	209˙033.40

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 Obiettivo del progetto (Objective)

'In this proposal I wish to test the hypothesis that immune cells of the Natural Killer (NK) lineage use similar mechanisms to regulate both invasive placental cells and invasive cancer cells. Trophoblast cells and NK cells appear to come into close contact at the fetal-maternal interface during early pregnancy both in human and mice. Trophoblast cells indeed invade deep into the uterus while maternal NK cells accumulate adjacent to the invading trophoblast. These immune cells are a unique population and are known as uterine NK (uNK) cells. The interactions between trophoblast and uNK cells most likely influence the tissue remodelling that results in increased blood flow necessary for fetal growth. Thus, these interactions are key to successful reproduction but the molecular mechanisms are unknown and are the focus of this proposal. Like human uNK cells, also mouse uNK cells express activating receptors, such as the Natural Cytotoxicity Receptor NKp46, which is coded by the Ncr1 gene and is conserved in human, mice and many other species. NKp46 is a key receptor to recognise cancer cells. The host laboratory (lead by F Colucci) has shown that NKp46-deficient mice are more prone to metastatic melanoma (JCI, 2009) and that mouse trophoblast cells may express NKp46 ligands (unpublished). Considering the invasive properties of trophoblast, the question we wish to address is whether NKp46 controls the extent of trophoblast invasion, thereby affecting spiral arteries remodelling and fetal-placental growth. To address this question, we will compare trophoblast invasion, spiral artery modification and fetal-placental growth in NKp46-sufficient and NKp46-deficient transgenic mice. The understanding of the molecular interactions between uNK cells and trophoblast will help define the role of uNK cells in reproduction and may have implications in cancer and transplantation.'