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Small RNA profiling of wildtype and Eri1-deficient mouse T cells

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. Eri1 was required for immune-mediated control of mouse cytomegalovirus (MCMV) infection. Ly49H+ NK cells deficient in Eri1 failed to expand efficiently during MCMV infection, and virus-specific responses were also diminished among Eri1–/– T cells. 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE31920 | GEO | 2012/07/11

SECONDARY ACCESSION(S): PRJNA145057

REPOSITORIES: GEO

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Small RNA profiling of wildtype and Eri1-deficient mouse T cells

Project description: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 3M-bM-^@M-^Y-to-5M-bM-^@M-^Y exoribonuclease that represses RNA interference, have a cell-intrinsic defect in NK cell development and maturation. Eri1M-bM-^@M-^S/M-bM-^@M-^S 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. Eri1 was required for immune-mediated control of mouse cytomegalovirus (MCMV) infection. Ly49H+ NK cells deficient in Eri1 failed to expand efficiently during MCMV infection, and virus-specific responses were also diminished among Eri1M-bM-^@M-^S/M-bM-^@M-^S T cells. 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 Eri1M-bM-^@M-^S/M-bM-^@M-^S T cells. Thus, mouse Eri1 regulates miRNA homeostasis in lymphocytes and is required for normal NK cell development and anti-viral immunity. Small RNA profiling from wildtype and Eri1-deficient mouse CD4+ T cells

2012-07-11 | E-GEOD-31920 | biostudies-arrayexpress

miRNA measurements in wildtype and Eri1-deficient Th cells

Project description: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 3M-bM-^@M-^Y-to-5M-bM-^@M-^Y exoribonuclease that represses RNA interference, have a cell-intrinsic defect in the homeostasis and terminal maturation of NK cells. Eri1M-bM-^@M-^S/M-bM-^@M-^S NK cells show delayed acquisition of Ly49 receptors in the bone marrow and a selective reduction in Ly49D and Ly49H activating receptors in the periphery. Furthermore, antigen-specific Ly49H+ NK cells deficient in Eri1 fail to expand efficiently in mouse cytomegalovirus (MCMV) infection. Consequently, we find that Eri1 is required for immune-mediated control of MCMV titers. In contrast to NK cells, T cells deficient in Eri1 differentiate into effectors that produce high levels of Th2 cytokines. Here we identify miRNAs as the major endogenous small RNA target of Eri1 in mouse lymphocytes. NK and T cells deficient in Eri1 display an approximately two-fold increase in all miRNAs. In Eri1-deficient T cells, ectopic expression of wildtype Eri1 is sufficient to rescue defects in both miRNA homeostasis and Th2 cytokine production. Thus mouse Eri1 negatively regulates miRNA homeostasis and is required to promote normal lymphocyte effector functions. One sample; one color design. These are six arrays from a study investigating the microRNA profile of wildtype and Eri1-deficient Th cells that is to published separately.

2012-07-10 | E-GEOD-32126 | biostudies-arrayexpress

miRNA measurements in wildtype and Eri1-deficient Th cells

Project description: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 the homeostasis and terminal maturation of NK cells. Eri1–/– NK cells show delayed acquisition of Ly49 receptors in the bone marrow and a selective reduction in Ly49D and Ly49H activating receptors in the periphery. Furthermore, antigen-specific Ly49H+ NK cells deficient in Eri1 fail to expand efficiently in mouse cytomegalovirus (MCMV) infection. Consequently, we find that Eri1 is required for immune-mediated control of MCMV titers. In contrast to NK cells, T cells deficient in Eri1 differentiate into effectors that produce high levels of Th2 cytokines. Here we identify miRNAs as the major endogenous small RNA target of Eri1 in mouse lymphocytes. NK and T cells deficient in Eri1 display an approximately two-fold increase in all miRNAs. In Eri1-deficient T cells, ectopic expression of wildtype Eri1 is sufficient to rescue defects in both miRNA homeostasis and Th2 cytokine production. Thus mouse Eri1 negatively regulates miRNA homeostasis and is required to promote normal lymphocyte effector functions.

2012-07-11 | GSE32126 | GEO

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Project description:Plasmacytoid dendritic cells (pDC) are the major source of type I IFN (IFN-I) in vivo during Murine Cytomegalovirus (MCMV) infection. This response requires pDC-intrinsic MyD88-dependent signaling by Toll Like Receptors 7/9. Provided that they express appropriate recognition receptors such as Ly49H, Natural Killer (NK) cells can directly sense and kill MCMV-infected cells. While MyD88- and Ly49H-dependent responses can contribute to MCMV control, the objective is to understand the relative importance of these 3 mechanisms. In order to decipher the relative impact of MyD88- and Ly49H-dependent mechanisms during MCMV infection, we performed a genome-wide expression analysis on total spleen of Ly49H-/-MyD88+/+, Ly49H-/-MyD88-/-, Ly49H+/+MyD88+/+ and Ly49H+/+MyD88-/- BALB/c mice at different time points after MCMV infection (d0, d1,5, d2, d3 and d6). This study includes data from the spleen BALB/c mice, under steady-state or MCMV condition at different time points. 2 to 5 mice for each mouse strain for each time point were used, and were hybridized on 5 separate batches of gene chips.

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Avidity Selection of Natural Killer Response to MCMV

Project description:Natural killer (NK) cells are innate lymphocytes that possess features of adaptive immunity, such as the ability to recognize specific antigen, among others. In MCMV infection, the engagement of a subset of NK cells expressing an activating receptor Ly49H with MCMV-derived glycoprotein m157 results in a clonal-like expansion and the generation of a small pool of long-lived memory cells with higher Ly49H expression than the naive Ly49H-expressing NK cell pool. In this study, we interrogate the transcriptional differences between NK cells that express high verus low levels of Ly49H early after infection.

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Natural killer cell sensing of infected cells compensates deficient Toll-like receptor but not IFN-I activity for mouse resistance to cytomegalovirus

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