Molecular targets of miR The results obtained on five evaluable patients, presented at the last American Society of Hematology ASH Meeting, showed that intra-tumor injection of MRG was well tolerated and demonstrated encouraging therapeutic improvements in cutaneous lesions and a significant decrease in systemic disease-related symptoms, such as pruritus [ ]. A miRPeli1-c-Rel pathway controls the generation and function of T follicular helper cells. Thus, other studies were focused on characterizing the role of additional genes deleted in del 5q MDSs. In a more recent study, the same authors explored the functional role of miRa and miRb in human dendritic cells. Experiments carried out using the virulent MBT strain support a permissive role for miR in the infection of macrophages by mycobacteria: Both DCs and monocytes are heterogeneous, with different populations displaying different effector and immunomodulatory functions. 
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Furthermore, the functional role drivdr their target genes was also carefully documented. LPS stimulation induces an increase not only of miRa, but also of miRb.
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A recent study explored the expression and function of miRb in human Treg and obtained evidence suggesting a functional role different from that described through the study of miR knockout mice. According to these findings, it was proposed that miRa and miR counter-regulate Tfh development [ 71 ]. Up-modulation or silencing of miRa expression, with mimics or antagomirs, in purified Treg, modified cytokine secretion, but failed to change the Treg function [ 57 ].
The fine tuning of miRa and miR expression in these cells is essential for an appropriate control of various essential immune functions, and usually, these two miRNAs act in an opposite way.
In a more recent study, the same authors explored the functional role of miRa and miRb in human dendritic cells. Expression and function of miR in various cell types of the immune system.
miR-146 and miR-155: Two Key Modulators of Immune Response and Tumor Development
Author information Article notes Copyright and License information Disclaimer. Pattern recognition receptors and inflammation.
Re-polarization drivre tumor-associated macrophages to pro-inflammatory M1 macrophages by microRNA Clinical role of microRNAs in cytogenetically normal acute myeloid leukemia: Distinct microRNA expression profiles in acute myeloid leukemia with common translocations.
Thus, Jurkin and coworkers have shown that plasmacytoid DCs express miRa at levels four-times higher than myeloid int-DCs [ 22 ]. This fundamental study thus indicated a key role of miR as a modulator of immune function.
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T helper lymphocytes Th can be subdivided into three subpopulations: MicroRNA confers encephalogenic potential to Th17 cells by promoting effector gene expression. AKT1 is indispensable for endotoxin tolerance generation and acts through a mechanism involving the suppression of miR and consequent up-modulation of its target SOCS1, induction of let-7e and reduced TLR4 expression [ 38 ].
Conflicts of Interest The authors declare no conflict of interest. The study of human Th1 cells showed the existence drivre a new direct molecular pathway through which miRa exerts an inhibitory effect on the differentiation of these cells. Thus, a phase I first-in human study was performed to evaluate the safety tolerability, pharmacokinetics and preliminary efficacy of MRG in patients with mycosis fungoides the most frequent type of CTCLs.
In fact, miRdeficient Tfh cells display reduced cell proliferation and differentiation and decreased CD40L expression [ 72 ]. MDS patients with a del 5q are characterized by some phenotypical features, including refractory anemia, neutropenia and thrombocytosis, associated with megakaryocytic dysplasia hypolobulated megakaryocytes.
The most frequent chromosome abnormality observed in MDSs consists of a deletion of chromosome 5q delOK 5q. While the role of miR in the regulation of Treg cell differentiation seems to be more defined, its role in regulating Treg suppressive function is less clear. Coordinated regulation of miR and miRa genes during induction of endotoxin tolerance in macrophage.
It is important to note the similarity of the phenotype of TRAF6 overexpressing mice with the phenotype of mIRa-deficient mice, except for platelet abnormalities absent in the miRa-deficient mice.
Finally, miRa was found to be indispensable for the development of endotoxin tolerance to intestinal bacteria in neonates [ 43 ].
Received May 12; Accepted Jun Importantly, miRa-5p and miRb-5p, here called miRa and miRb, share a seed sequence and are, therefore, predicted to target the same set of genes. More than conserved miR are encoded by the mammalian genome.
Neighboring genes in del 5q myelodysplastic syndrome.
An important molecular consequence of del 5q is an increased expression of TRAF6, resulting from miRa haploinsufficiency [ ]. The kinase Akt1 controls macrophage response to lipopysaccharide by regulating microRNAs. In fact, Malmhall and coworkers observed a reduced allergic reaction at the level of lungs in allergen-challenged miRdeficient mice [ 67 ]. These miRs arise from different genetic loci and are generated via different routes of RNA processing: Author Contributions All of the authors have significantly contributed to writing the paper.
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