Activation of CD8 super(+) Regulatory T Cells by Human Placental Trophoblasts

The immunological basis by which a mother tolerates her semi-allogeneic fetus remains poorly understood. Several mechanisms are likely to contribute to this phenomenon including active immune regulation by regulatory T cells. In this article, we report that human placental trophoblasts activate a cl...

Full description

Saved in:
Bibliographic Details
Published inThe Journal of immunology (1950) Vol. 174; no. 12; pp. 7539 - 7547
Main Authors Shao, Ling, Jacobs, Adam R, Johnson, Valrie V, Mayer, Lloyd
Format Journal Article
LanguageEnglish
Published 01.06.2005
Online AccessGet full text

Cover

Loading…
More Information
Summary:The immunological basis by which a mother tolerates her semi-allogeneic fetus remains poorly understood. Several mechanisms are likely to contribute to this phenomenon including active immune regulation by regulatory T cells. In this article, we report that human placental trophoblasts activate a clonal population of CD8 super(+) T cells with regulatory function. These cells are not MHC class I restricted, but require costimulation through a member of the carcinoembryonic Ag family present on early gestation trophoblasts. These regulatory T cells express the mucosal markers CD101 and CD103 and display selective usage of the TCR gene V beta 9. CD8 super(+) T cells isolated from the peripheral blood of pregnant mothers (16-28 wk) also demonstrate expansions in the same V beta family (V beta 9), signaling a possible role for these cells in preventing fetal rejection in vivo. We have previously characterized a subset of CD8 super(+) regulatory T cells activated by the combination of the nonclassical class I molecule CD1d and a costimulatory molecule of the carcinoembryonic Ag family present on the intestinal epithelium. These data support the concept that distinct regulatory T cell populations exist at different sites and may be regulated locally by unique restriction elements, costimulatory signals, and Ags.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
content type line 23
ObjectType-Feature-1
ISSN:0022-1767