This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Barber, E. M. Articles by Pollard, J. W. Search for Related Content PubMed PubMed Citation Articles by Barber, E. M. Articles by Pollard, J. W.

 Previous Article  |  Next Article 

Infection and Immunity, October 2005, p. 6322-6331, Vol. 73, No. 10
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.10.6322-6331.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Th1 Cytokines Are Essential for Placental Immunity to Listeria monocytogenes

Department of Developmental and Molecular Biology and Obstetrics and Gynecology and Women's Health,¹ Department of Epidemiology and Social Medicine,² Center for the Study of Reproductive Biology and Women's Health, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461³

Received 3 February 2005/ Returned for modification 8 April 2005/ Accepted 16 June 2005

The fetal allograft poses an immunological challenge: how is it protected while immunity to pathogens, particularly those that replicate in the placenta, is maintained? Several theories have been proposed to explain this fetal protection, including a pregnancy-based bias towards a Th2 rather than Th1 cytokine profile in order to avoid generating cytotoxic T cells that could threaten the fetus. Listeria monocytogenes preferentially replicates in the placenta and systemically requires a Th1 response for sterile eradication. In the placenta, the Th1 cytokines tumor necrosis factor alpha (TNF-) and gamma interferon (IFN-) are also synthesized in response to this pathogen, without fetal loss. Here we show, by using mice homozygous for null mutations in either the cytokine or cytokine receptor genes, a requirement for both TNF- and IFN- signaling for an effective placental immune response to L. monocytogenes. However, T cells were not recruited to the placenta. Genetic studies in which the fetal component of the placenta was genetically different from the mother indicated that both the production of and response to these cytokines were maternal. Despite the requirement for these cytokines, the early recruitment of neutrophils to the placenta was normal. Consequently, the bacterium appeared to be delayed in its colonization of this organ and did not fully gain hold until 72 h postinfection. These data show a requirement for Th1 cytokines during pregnancy for effective immunity and indicate that a bias away from Th1 cytokine synthesis is not a necessary prerequisite of pregnancy.

Editor: J. B. Bliska

This article has been cited by other articles:

• Rosbottom, A., Gibney, E. H., Guy, C. S., Kipar, A., Smith, R. F., Kaiser, P., Trees, A. J., Williams, D. J. L. (2008). Upregulation of Cytokines Is Detected in the Placentas of Cattle Infected with Neospora caninum and Is More Marked Early in Gestation When Fetal Death Is Observed. Infect. Immun. 76: 2352-2361 [Abstract] [Full Text]