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J Reprod Immunol. 2007 Dec;76(1-2):30-9. Epub 2007 Nov 1.

Inadequate tolerance induction may induce pre-eclampsia.

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1
Department of Obstetrics and Gynecology, University of Toyama, 2630 Sugitani, Toyama, Japan; Center of Excellence (COE) 21st Program, Japan. s30saito@med.u-toyama.ac.jp

Abstract

The fetus is semi-allograft to the maternal host; therefore, a system of tolerance must be present during pregnancy. Epidemiological findings support a relationship between pre-eclampsia and the failure of tolerance induction. For induction of major histocompatibility complex (MHC) class I-specific tolerance, long-term exposure to seminal fluid, which contains paternal soluble MHC class I antigens, may induce paternal MHC class I-specific tolerance. Furthermore, soluble HLA-G1, which induces the deletion of CD8(+) T-cells, and the combination of maternal killer-immunoglobulin-like receptors (KIR) on NK cells and fetal HLA-C, which affects the balance between inhibition and activation signals of NK cells, regulatory CD8(+) T cells, and regulatory NK cells, may play very important roles in the induction of MHC class I-specific tolerance. On the other hand, exposure to sperm, which express paternal HLA-DR, and trophoblastic debris, which contain intracellular fetal HLA-DR, may induce paternal MHC class II-specific tolerance. In this process, CD4(+)CD25(+) regulatory T (Treg)-cells play central roles. In this review, we discuss the relationship between the risk of pre-eclampsia and tolerance induction.

PMID:
17935792
DOI:
10.1016/j.jri.2007.08.002
[Indexed for MEDLINE]
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