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Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation
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Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation

Published on: September 20, 2017

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IL-10 regulates Aicda expression through miR-155

Kirsten A Fairfax1, Michael P Gantier1, Fabienne Mackay1

  • 1*Faculty of Medicine, Department of Immunology, Monash University, Prahran, and Department of Molecular and Translational Science, Monash University, Clayton, Victoria, Australia; The Department of Experimental Medicine, University of Melbourne, Parkville, Victoria, Australia; Division of Molecular Medicine, The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia; Centre for Cancer Research, Monash Institute of Medical Research-Prince Henry's Institute of Medical Research, Clayton, Victoria, Australia; and School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Ireland.

Journal of Leukocyte Biology
|November 9, 2014
PubMed

Aicda is a critical component of antibody class-switching in B cells. In this work, we study the impact of TLR4 activation and IL-10 stimulation on Aicda expression in B cells. Through the global analysis of miRNAs in response to TLR4 activation, in combination with IL-10 stimulation, we identified that IL-10 can suppress TLR4-induced miR-155 expression, an effect that resulted in enhanced Aicda expression. Furthermore, when preventing miR-155 control of Aicda expression, by genetic mutation of its target site in the Aicda mRNA, IL-10 could further potentiate Aicda expression. Given that miR-155 expression is lost, and expression levels of both Aicda and IL-10 are high in diseases, such as Burkitt's lymphoma, our results suggest a stringent and sophisticated control of Aicda by a novel IL-10/miR-155 axis, where the imbalance of IL-10 and/or miR-155 may contribute to disease pathogenesis.

Keywords:
AIDB cellTLR4antibody class-switchinginterleukinmiRNA

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