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.

Item Type:	Refereed Article
Keywords:	AID, B cell, TLR4, antibody class-switching, interleukin, miRNA
Research Division:	Biological Sciences
Research Group:	Biochemistry and cell biology
Research Field:	Cell development, proliferation and death
Objective Division:	Health
Objective Group:	Clinical health
Objective Field:	Clinical health not elsewhere classified
UTAS Author:	Fairfax, KA (Dr Kirsten Fairfax)
ID Code:	134781
Year Published:	2015
Web of Science® Times Cited:	16
Deposited By:	Menzies Institute for Medical Research
Deposited On:	2019-09-04
Last Modified:	2019-10-18
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