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Original Article

Interferon Contributes to Initiation of Uterine Vascular Modification, Decidual Integrity, and Uterine Natural Killer Cell Maturation during Normal Murine Pregnancy

^a Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada N1G 2W1
^b Department d' Immunologie, Institut Pasteur, 75724 Paris, France
Dept. of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada N1G 2W1.519-767-1450519-824-8800 ext. 4956

aashkar{at}uoguelph.ca

The dominant lymphocytes in human and murine implantation sites are transient, pregnancy-associated uterine natural killer (uNK) cells. These cells are a major source of interferon (IFN)-. Implantation sites in mice lacking uNK cells (alymphoid recombinase activating gene [RAG]-2^–/– common cytokine receptor chain [_c]^–/–) or IFN- signaling (IFN-^–/– or IFN-R^–/–) fail to initiate normal pregnancy-induced modification of decidual arteries and display hypocellularity or necrosis of decidua. To investigate the functions of uNK cell–derived IFN- during pregnancy, RAG-2^–/–_c^–/– females were engrafted with bone marrow from IFN-^–/– mice, IFN- signal-disrupted mice (IFN-R^–/– or signal transducer and activator of transcription [Stat]-1^–/–), or from mice able to establish normal uNK cells (severe combined immunodeficient [SCID] or C57BL/6). Mated recipients were analyzed at midgestation. All grafts established uNK cells. Grafts from IFN-^–/– mice did not reverse host vascular or decidual pathology. Grafts from all other donors promoted modification of decidual arteries and decidual cellularity. Grafts from IFN-R^–/– or Stat-1^–/– mice overproduced uNK cells, all of which were immature. Grafts from IFN-^–/–, SCID, or C57BL/6 mice produced normal, mature uNK cells. Administration of murine recombinant IFN- to pregnant RAG-2^–/–_c^–/– mice initiated decidual vessel modification and promoted decidual cellularity in the absence of uNK cells. These in vivo findings strongly suggest that uNK cell–derived IFN- modifies the expression of genes in the uterine vasculature and stroma, which initiates vessel instability and facilitates pregnancy-induced remodeling of decidual arteries.

Key Words: interferon signaling • uterine lymphocytes • decidual spiral arteries • bone marrow transplantation • tumor necrosis factor

© 2000 The Rockefeller University Press

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This article has been cited by other articles:

• Redline, R. W. (2000). Role of Uterine Natural Killer Cells and Interferon {gamma} in Placental Development. JEM 192: f1-f4 [Full Text]  

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