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Tolerance of the fetus by the maternal immune system: role of inflammatory mediators at the feto-maternal interface.

Kanellopoulos-Langevin C, Caucheteux SM, Verbeke P, Ojcius DM - Reprod. Biol. Endocrinol. (2003)

Bottom Line: The adaptive immune system of placental mammals has evolved to tolerate the fetus.Rejection of the fetus by adaptive immune responses is therefore a rare event, with abortion being caused more frequently by inflammation in the placenta.This review will cover recent aspects of immune privilege and the innate immune system at the feto-maternal interface, citing examples of the role played by microbial infections in fetal demise.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institut Jacques Monod, CNRS UMR 7592, Universités Paris 6 & 7, 2 place Jussieu, 75251 Paris Cedex 5, France. kanellopoulos@ijm.jussieu.fr

ABSTRACT
The adaptive immune system of placental mammals has evolved to tolerate the fetus. Rejection of the fetus by adaptive immune responses is therefore a rare event, with abortion being caused more frequently by inflammation in the placenta. This review will cover recent aspects of immune privilege and the innate immune system at the feto-maternal interface, citing examples of the role played by microbial infections in fetal demise.

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Cross-talk between fetal trophoblast and maternal macrophages and neutrophils during placental infection by Listeria. MΦ: macrophage; CSF-1: colony stimulating factor 1; KC: cytokine-induced neutrophil chemoattractant; (MIP)-2: macrophage inflammatory protein-2.
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Figure 3: Cross-talk between fetal trophoblast and maternal macrophages and neutrophils during placental infection by Listeria. MΦ: macrophage; CSF-1: colony stimulating factor 1; KC: cytokine-induced neutrophil chemoattractant; (MIP)-2: macrophage inflammatory protein-2.

Mentions: In mice, during infection with bacteria such as Listeria monocytogenes or Chlamydia trachomatis, maternal neutrophils are recruited to the fetomaternal interface and act as the main immune effector cells against the bacteria. The macrophage growth factor, colony stimulating factor (CSF)-1, is produced in large quantities by the uterine epithelium during pregnancy, and induces trophoblasts to synthesize neutrophil chemoattractants, cytokine-induced neutrophil chemoattractant (KC) (CXCL1), and macrophage inflammatory protein (MIP)-2 (CXCL2) [40] (Fig. 3). In the absence of CSF-1, neutrophils are not recruited and bacterial infection is unrestrained, leading to fetal demise. In parallel, the macrophage migration inhibitory factor (MIF), which is expressed in the human endometrium in early pregnancy, inhibits NK cell-mediated cytolysis and could thus contribute to immune privilege at the feto-maternal interface. Conversely, MIF also stimulates macrophage phagocytosis and secretion of TNFα and IL-1β, which could lead to recruitment and maintenance of a pool of activated phagocytes in the endometrium [41].


Tolerance of the fetus by the maternal immune system: role of inflammatory mediators at the feto-maternal interface.

Kanellopoulos-Langevin C, Caucheteux SM, Verbeke P, Ojcius DM - Reprod. Biol. Endocrinol. (2003)

Cross-talk between fetal trophoblast and maternal macrophages and neutrophils during placental infection by Listeria. MΦ: macrophage; CSF-1: colony stimulating factor 1; KC: cytokine-induced neutrophil chemoattractant; (MIP)-2: macrophage inflammatory protein-2.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC305337&req=5

Figure 3: Cross-talk between fetal trophoblast and maternal macrophages and neutrophils during placental infection by Listeria. MΦ: macrophage; CSF-1: colony stimulating factor 1; KC: cytokine-induced neutrophil chemoattractant; (MIP)-2: macrophage inflammatory protein-2.
Mentions: In mice, during infection with bacteria such as Listeria monocytogenes or Chlamydia trachomatis, maternal neutrophils are recruited to the fetomaternal interface and act as the main immune effector cells against the bacteria. The macrophage growth factor, colony stimulating factor (CSF)-1, is produced in large quantities by the uterine epithelium during pregnancy, and induces trophoblasts to synthesize neutrophil chemoattractants, cytokine-induced neutrophil chemoattractant (KC) (CXCL1), and macrophage inflammatory protein (MIP)-2 (CXCL2) [40] (Fig. 3). In the absence of CSF-1, neutrophils are not recruited and bacterial infection is unrestrained, leading to fetal demise. In parallel, the macrophage migration inhibitory factor (MIF), which is expressed in the human endometrium in early pregnancy, inhibits NK cell-mediated cytolysis and could thus contribute to immune privilege at the feto-maternal interface. Conversely, MIF also stimulates macrophage phagocytosis and secretion of TNFα and IL-1β, which could lead to recruitment and maintenance of a pool of activated phagocytes in the endometrium [41].

Bottom Line: The adaptive immune system of placental mammals has evolved to tolerate the fetus.Rejection of the fetus by adaptive immune responses is therefore a rare event, with abortion being caused more frequently by inflammation in the placenta.This review will cover recent aspects of immune privilege and the innate immune system at the feto-maternal interface, citing examples of the role played by microbial infections in fetal demise.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institut Jacques Monod, CNRS UMR 7592, Universités Paris 6 & 7, 2 place Jussieu, 75251 Paris Cedex 5, France. kanellopoulos@ijm.jussieu.fr

ABSTRACT
The adaptive immune system of placental mammals has evolved to tolerate the fetus. Rejection of the fetus by adaptive immune responses is therefore a rare event, with abortion being caused more frequently by inflammation in the placenta. This review will cover recent aspects of immune privilege and the innate immune system at the feto-maternal interface, citing examples of the role played by microbial infections in fetal demise.

Show MeSH
Related in: MedlinePlus