MiRNA measurements in wildtype and Eri1-deficient Th 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 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.

ORGANISM(S): Mus musculus

SUBMITTER: Andrea Barczak 

PROVIDER: E-GEOD-32126 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress