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In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells

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Published on: January 20, 2019

A methyl-deficient diet modifies early B cell development.

Toshiaki Kurogi¹, Hiroko Inoue, Yun Guo

¹Department of Immunology, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.

Pathobiology : Journal of Immunopathology, Molecular and Cellular Biology

|April 18, 2012

Summary

Methyl donor deficiency impacts early B cell development in mice. A methyl-deficient diet altered immune cell populations and gene expression, affecting B cell maturation through epigenetic modifications.

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Area of Science:

Immunology
Epigenetics
Developmental Biology

Background:

Epigenetic regulation relies on methyl group donors for DNA and histone methylation.
The impact of methyl donor deficiency on immune system epigenetics is not well understood.

Purpose of the Study:

To investigate lymphocyte development and DNA methylation changes in mice fed a methyl-deficient diet (MDD).

Main Methods:

Mice were fed either a methyl-sufficient diet (MSD) or MDD for 5 months.
Flow cytometry analyzed immune cell populations.
In vitro OP9 co-culture system assessed B cell development defects.
Quantitative mRNA expression and semi-quantitative RT-PCR analyzed gene expression.
Histone and DNA methylation profiles were measured.

Main Results:

MDD led to decreased immature B cells and increased pro/pre-B cells in bone marrow.
B cell fraction from MDD mice showed intrinsic developmental defects.
Expression of ADA, EBF1, DNTT, and Pax5 mRNA was downregulated in MDD mice.
Histone methylation (H3K4me3) decreased at Pax5 and EBF1 promoters.
Polycomb group gene expression levels were altered.

Conclusions:

Methyl-deficient diets can affect early B cell development in bone marrow via epigenetic alterations.
Specific gene downregulation and changes in histone methylation are implicated in MDD-induced B cell defects.