perhaps an answer to a long-standing question

Why doesn't a mother's immune system reject a fetus?  Progress on an answer really neat!

snip

 

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The research team has discovered that the onset of pregnancy causes the genes that are responsible for recruiting immune cells to sites of inflammation to be turned off within the decidua. As a result of these changes, T cells are not able to accumulate inside the decidua and therefore do not attack the fetus and placenta.

Specifically, they revealed that the implantation of an embryo changes the packaging of certain chemokine genes in the nuclei of the developing decidua’s stromal cells. The change in the DNA packaging permanently deactivates, or “silences,” the chemokine genes. Consequently, the chemokines are not expressed and T cells are not recruited to the site of embryo implantation.

Also of note, the observed change in the DNA packaging was a so-called ‘epigenetic’ modification, meaning a modification that changes gene expression without the presence of a hereditable gene mutation.

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Chemokine Gene Silencing in Decidual Stromal Cells

Limits T Cell Access to the Maternal-Fetal Interface

1. Patrice Nancy¹, 
2. Elisa Tagliani¹, 
3. Chin-Siean Tay¹, 
4. Patrik Asp²,*, 
5. David E. Levy¹,², 
6. Adrian Erlebacher¹,²,^†

+Author Affiliations

1. ¹Department of Pathology, New York University School of Medicine, New York, NY 10016, USA.
2. ²New York University Cancer Institute, New York University School of Medicine, New York, NY 10016, USA.

ABSTRACT

The chemokine-mediated recruitment of effector T cells to sites of inflammation is a central feature of the immune response. The extent to which chemokine expression levels are limited by the intrinsic developmental characteristics of a tissue has remained unexplored. We show in mice that effector T cells cannot accumulate within the decidua, the specialized stromal tissue encapsulating the fetus and placenta. Impaired accumulation was in part attributable to the epigenetic silencing of key T cell–attracting inflammatory chemokine genes in decidual stromal cells, as evidenced by promoter accrual of repressive histone marks. These findings give insight into mechanisms of fetomaternal immune tolerance, as well as reveal the epigenetic modification of tissue stromal cells as a modality for limiting effector T cell trafficking.