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Related Experiment Video

Updated: Jul 8, 2026

Isolation of Leukocytes from the Human Maternal-fetal Interface

Isolation of Leukocytes from the Human Maternal-fetal Interface

Published on: May 21, 2015

Transient decrease in interleukin-7 availability arrests B lymphopoiesis during pregnancy.

Nabil Bosco¹, Rhodri Ceredig, Antonius Rolink

¹Department of Clinical and Biological Sciences (DKBW), Division of Molecular Immunology, Center for Biomedicine, University of Basel, Basel, Switzerland.

European Journal of Immunology

|January 19, 2008

Summary

This summary is machine-generated.

Pregnancy temporarily halts mouse B lymphopoiesis by reducing IL-7 availability, not by depleting precursors. Exogenous IL-7 administration restores B cell development in pregnant mice.

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Last Updated: Jul 8, 2026

Isolation of Leukocytes from the Human Maternal-fetal Interface

Isolation of Leukocytes from the Human Maternal-fetal Interface

Published on: May 21, 2015

Isolation of Leukocytes from the Murine Tissues at the Maternal-Fetal Interface

Isolation of Leukocytes from the Murine Tissues at the Maternal-Fetal Interface

Published on: May 21, 2015

Area of Science:

Immunology
Developmental Biology
Hematopoiesis

Background:

B lymphopoiesis, the development of B lymphocytes, is known to be transiently arrested during pregnancy in mice.
This arrest was previously hypothesized to result from the depletion of a hormone-sensitive bone marrow precursor.

Purpose of the Study:

To investigate the precise mechanisms by which pregnancy affects mouse B cell development.
To identify the specific progenitor cells involved and the molecular regulators of this process.

Main Methods:

Utilized a combination of in vitro and in vivo experimental approaches.
Conducted detailed phenotypic and functional analyses of bone marrow progenitor cells.
Characterized the early progenitor with lymphoid and myeloid potential (EPLM) as the immediate precursor to pre-B1 cells.

Main Results:

B cell development was observed to be blocked at the EPLM-to-pre-B1 transition during late pregnancy in mice.
This developmental block correlated with a significant reduction in Interleukin-7 (IL-7) levels, caused by downregulated IL-7 gene transcription.
Administration of exogenous IL-7 successfully rescued B lymphopoiesis in pregnant mice, demonstrating its critical role.

Conclusions:

Pregnancy-induced dampening of bone marrow B cell development is mediated by hormonal fine-tuning of IL-7 availability.
The mechanism involves reduced IL-7 levels rather than direct depletion of hormone-sensitive B cell precursors.