Article title: A new role for microRNAs, as ligands of Toll-like Receptors
Authors: Fabbri, M., Paone, A., Calore, F., Galli, R. Croce, C.M.
Journal: RNA Biology
Bibliometrics: Volume 10, Number 02, pages 169-174
DOI: https://doi.org/10.4161/rna.23144
When the above article was first published online, citation of the following referenced articles were missing.
[81] Stoorvogel W. (2012) Functional transfer of microRNA by exosomes, Blood. 119:646-648. https://doi.org/10.1182/blood-2011-11-389478
[82] Hornung V, Barchet W, Schlee M, Hartmann G. (2008) RNA recognition via TLR7 and TLR8, Handbook of Experimental Pharmacology. 183:71-86. DOI: 10.1007/978-3-540-72167-3_4
[83] Schön MP, Schön M. (2008) TLR7 and TLR8 as targets in cancer therapy, Oncogene 27:190-199. doi: 10.1038/sj.onc.1210913
The above references should be added to the following places within the published RNA Biology review:
Page 170: Montecalvo and coworkers showed “that dendritic cells (DCs) secrete exosomes that are loaded with distinct sets of” miRNAs, “dependent on the status of DC activation” and that such “exosomes can fuse with target cells, thereby delivering their membranous and cytosolic contents”. [81].
Page 171: “The TLR family consists of 10 members (13 in mice), which enable innate immune cells and other specialized cell subsets such as epithelial cells to respond to a variety of pathogen-associated molecular patterns (PAMPs) [39]. TLR3, TLR7, TLR8 and TLR9 form a subgroup of TLRs” [82] for structural and functional similarities. All of them, in fact, recognize viral nucleic acid and are “located in the endosomal membrane.” [82]
Page 171: “TLR7 and TLR8 were initially identified as receptors for antiviral small molecules such as imidazoquinoline derivates” [42,43,82], but subsequently “were found to be responsible for the detection of ssRNA derived from the human immunodeficiency virus (HIV) and the influenza virus [40,41,82]”.
Page 171: “showed that both TLR7 and TLR8 transfer responsiveness to ssRNA, but in mice this is true only for TLR7 [40,41,82]”.
Page 171: “followed by the formation of a complex with IRAK1, IRAK4 and TRAF6, which results in NF-kB (nuclear factor-kappa B) activation” [82].
Page 171: “scientific and clinical interest in TLR7 and TLR8 for cancer biology has originated from the discovery of antitumoral activity of some small-molecule compounds [61] which have been shown to act as agonists for one or both receptors [43,62]. Most of the findings concerning the antitumoral mode of action of TLR7/8 agonists have been obtained with the nucleoside analogue imiquimod [63]. Imiquimod activates preferentially TLR7; its agonistic activity on TLR8 appears to be much weaker [64]. Another molecule named Resiquimod is a selective ligand for TLR7 in mice and for TLR7 and TLR8 in humans. Resiquimod induces more pronounced cytokine secretion, macrophage activation and enhancement of cellular immunity as compared to imiquimod [65,66]. Gardiquimod is another imidazoquinoline derivative that, similar to imiquimod, induces activation of nuclear factor (NF)-κB in cells expressing human or murine TLR7. At high concentrations (that is, ≥ 3 μg ml−1), gardiquimod also activates TLR8.” [83]. “imiquimod induces expression of proinflammatory cytokines including IFNα, TNFα, IL-2, -6, -8, -12, G-CSF and GM-CSF, as well as chemokines such as CCL3 (MIP-1α), CCL4 (MIP-1β) and CCL2 (MCP-1) [67-69, 83]”.
Page 171: “In addition to the NF-κB-mediated transcription of proinflammatory mediators, it appears that TLR7- (and TLR8)-agonistic activities of imiquimod induce some proinflammatory cytokines, such as IFNγ, in a NF-κB-independent fashion. The known functions of these mediators explain, at least in part, many cellular responses to imiquimod including activation and chemotactic properties on dendritic cells and their precursors as well as on cytotoxic T-lymphocytes and other immune cells” [83].
Reference [51] in the published review was also insufficiently cited as the source of text in the following passages:
Page 171: “NF-kB plays a critical role in the development of tumors and in the context of cronic inflammation [44,45,51]”. “Although TLR expression was first observed in immune cells, several reports have described the expression of TLRs in non-malignant and malignant epithelial cells [51]”.
Page 171: “Several studies strongly suggest that chronic inflammation (i.e., chronic bronchitis, chronic obstructive diseases, emphysema, asbestos, or tobacco smoke) increases the risk of carcinogenesis [59,60]. Lungs are frequently exposed to RNA viruses (such as respiratory syncytial and influenza viruses) and pathogens that are recognized by TLR7 and TLR8 [40,42], which suggests that these TLRs are present on lung epithelial cells [51]”. “A link between TLR7 and TLR8 signaling and inflammation, tumor growth, and chemoresistance” has been observed [51].
Page 171: “These data emphasize that TLR signaling can directly interfere with the tumor cell either by increasing cell survival or by inducing resistance to cell death” [51].
Reference [70] in the published review was also insufficiently cited as the source of text in the following passage:
Page 171: “nanometric protamine-RNA particles induce production of IFN-a, whereas micrometric particles mainly induce the production of TNF-α in human immune cells. This difference is explained by the fact that nanoparticles (but not microparticles) are selectively phagocytosed by pDCs, which produce IFN- α, whereas monocytes (that mainly produce TNF- α) have a higher activation threshold than pDCs” [70].
Finally, reference [34] was missing as the source of text in the following passage:
Page 170: “miRNAs were expressed at higher levels in exosomes” [34] …. “that some miRNAs may be uniquely packed into exosomes” [34].
This correction notice amends the version of record by adding in the missing references.