Eri1 regulates microRNA homeostasis and mouse natural killer cell development and anti-viral function (115.9)

Abstract Natural killer (NK) cells play a critical role in early host defense to infected and transformed cells. Here we show that mice deficient in Eri1, a conserved 3’-to-5’ exoribonuclease that represses RNA interference, have a cell-intrinsic defect in NK cell development and maturation. Eri1-/-...

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Published inThe Journal of immunology (1950) Vol. 188; no. 1_Supplement; pp. 115 - 115.9
Main Authors Ansel, K Mark, Thomas, Molly, Abdul-Wajid, Sarah, Panduro, Marisella, Babiarz, Joshua, Rajaram, Misha, Woodruff, Prescott, Lanier, Lewis, Heissmeyer, Vigo
Format Journal Article
LanguageEnglish
Published 01.05.2012
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Summary:Abstract Natural killer (NK) cells play a critical role in early host defense to infected and transformed cells. Here we show that mice deficient in Eri1, a conserved 3’-to-5’ exoribonuclease that represses RNA interference, have a cell-intrinsic defect in NK cell development and maturation. Eri1-/- NK cells displayed delayed acquisition of Ly49 receptors in the bone marrow and a selective reduction in Ly49D and Ly49H activating receptors in the periphery. Furthermore, Ly49H+ NK cells deficient in Eri1 failed to expand efficiently during mouse cytomegalovirus (MCMV) infection. Consequently, Eri1 was required for immune-mediated control of MCMV. We identified miRNAs as the major endogenous small RNA target of Eri1 in mouse lymphocytes. Both NK and T cells deficient in Eri1 displayed a global, sequence-independent increase in miRNA abundance. Ectopic Eri1 expression rescued defective miRNA expression in mature Eri1-/- T cells. Thus mouse Eri1 regulates miRNA homeostasis in lymphocytes and is required for normal NK cell development and anti-viral immunity.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.188.Supp.115.9