IL-10 regulates Aicda expression through miR-155

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10 Citations (Scopus)

Abstract

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.
Original languageEnglish
Pages (from-to)71 - 78
Number of pages8
JournalJournal of leukocyte biology
Volume97
Issue number1
DOIs
Publication statusPublished - 2015

Cite this

@article{1ea42c56377d4835b3652f879db82cf2,
title = "IL-10 regulates Aicda expression through miR-155",
abstract = "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.",
author = "Kirsten Fairfax and Gantier, {Michael Paul Marie} and Fabienne Mackay-Fisson and Williams, {Bryan Raymond George} and Claire McCoy",
year = "2015",
doi = "10.1189/jlb.2A0314-178R",
language = "English",
volume = "97",
pages = "71 -- 78",
journal = "Journal of leukocyte biology",
issn = "0741-5400",
publisher = "Society for Leukocyte Biology",
number = "1",

}

IL-10 regulates Aicda expression through miR-155. / Fairfax, Kirsten; Gantier, Michael Paul Marie; Mackay-Fisson, Fabienne; Williams, Bryan Raymond George; McCoy, Claire.

In: Journal of leukocyte biology, Vol. 97, No. 1, 2015, p. 71 - 78.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - IL-10 regulates Aicda expression through miR-155

AU - Fairfax, Kirsten

AU - Gantier, Michael Paul Marie

AU - Mackay-Fisson, Fabienne

AU - Williams, Bryan Raymond George

AU - McCoy, Claire

PY - 2015

Y1 - 2015

N2 - 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.

AB - 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.

UR - http://www.jleukbio.org/content/97/1/71.full.pdf+html

U2 - 10.1189/jlb.2A0314-178R

DO - 10.1189/jlb.2A0314-178R

M3 - Article

VL - 97

SP - 71

EP - 78

JO - Journal of leukocyte biology

JF - Journal of leukocyte biology

SN - 0741-5400

IS - 1

ER -