First Author | Zhang NN | Year | 2008 |
Journal | Proc Natl Acad Sci U S A | Volume | 105 |
Issue | 30 | Pages | 10553-8 |
PubMed ID | 18650396 | Mgi Jnum | J:139016 |
Mgi Id | MGI:3807111 | Doi | 10.1073/pnas.0804895105 |
Citation | Zhang NN, et al. (2008) RIG-I plays a critical role in negatively regulating granulocytic proliferation. Proc Natl Acad Sci U S A 105(30):10553-8 |
abstractText | RIG-I has been implicated in innate immunity by sensing intracellular viral RNAs and inducing type I IFN production. However, we have found a significant RIG-I induction in a biological setting without active viral infection-namely, during RA-induced terminal granulocytic differentiation of acute myeloid leukemias. Here, we present evidence that a significant Rig-I induction also occurs during normal myelopoiesis and that the disruption of the Rig-I gene in mice leads to the development of a progressive myeloproliferative disorder. The initiation of progressive myeloproliferative disorder is mainly due to an intrinsic defect of Rig-I(-/-) myeloid cells, which are characterized by a reduced expression of IFN consensus sequence binding protein, a major regulator of myeloid differentiation. Thus, our study reveals a critical regulatory role of Rig-I in modulating the generation and differentiation of granulocytes. |