Special Issue "Non-Coding RNA and the Immune System"

A special issue of Non-Coding RNA (ISSN 2311-553X).

Deadline for manuscript submissions: closed (28 February 2019).

Special Issue Editor

Dr. Dimitris Lagos
E-Mail Website
Guest Editor
Hull York Medical School and York Biomedical Research Institute, University of York, Wentworth Way, York YO10 5DD, UK
Interests: non-coding RNAs in immunity; immune gene expression; non-coding RNA biogenesis and mechanisms of action

Special Issue Information

Dear Colleagues,

Mammalian genomes are characterised by high prevalence of non-coding RNA (ncRNA) transcripts when compared to other species. It has been proposed that this correlates with the increased complexity of mammals. Undoubtedly, the mammalian immune system is a major contributor to this complexity. This Special Issue will aim to capture and showcase diverse aspects of our current understanding of how ncRNAs underpin complexity of the mammalian immune system.

Manuscripts on the following topics will be welcome:

  • ncRNAs in immune development, differentiation, and lineage plasticity, maintenance, and commitment
  • ncRNAs in infection, immunity, and host–pathogen interactions
  • ncRNAs in chronic inflammation, resolution, and fibrosis
  • Shaping immune transcriptomes through RNA–binding protein/ncRNA interactions
  • Infection exposure as a driver of lncRNA evolution in immune cells

Dr. Dimitris Lagos
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Non-Coding RNA is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • microRNAs
  • Long ncRNAs (lncRNAs)
  • circular RNAs (circRNAs)
  • RNA-binding proteins (RBPs)
  • Lineage commitment and plasticity
  • Infection, immunity, and host–pathogen interactions
  • Chronic inflammation, resolution, and fibrosis

Published Papers (4 papers)

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Review

Open AccessFeature PaperReview
Long Non-Coding RNA Function in CD4+ T Cells: What We Know and What Next?
Non-Coding RNA 2019, 5(3), 43; https://doi.org/10.3390/ncrna5030043 - 12 Jul 2019
Abstract
The non-coding genome has previously been regarded as “junk” DNA; however, emerging evidence suggests that the non-coding genome accounts for some of the greater biological complexity observed in mammals. Research into long non-coding RNAs (lncRNAs) has gathered speed in recent years, and a [...] Read more.
The non-coding genome has previously been regarded as “junk” DNA; however, emerging evidence suggests that the non-coding genome accounts for some of the greater biological complexity observed in mammals. Research into long non-coding RNAs (lncRNAs) has gathered speed in recent years, and a growing body of evidence has implicated lncRNAs in a vast range of cellular functions including gene regulation, chromosome organisation and splicing. T helper cells offer an ideal platform for the study of lncRNAs given they function as part of a complex cellular network and undergo remarkable and finely regulated gene expression changes upon antigenic stimulation. Using various knock down and RNA interaction studies several lncRNAs have been shown to be crucial for T helper cell differentiation, activation and function. Given that RNA targeting therapeutics are rapidly gaining attention, further understanding the mechanistic role of lncRNAs in a T helper context is an exciting area of research, as it may unearth a wide range of new candidate targets for treatment of CD4+ mediated pathologies. Full article
(This article belongs to the Special Issue Non-Coding RNA and the Immune System)
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Open AccessFeature PaperReview
MicroRNAs in Neuroinflammation: Implications in Disease Pathogenesis, Biomarker Discovery and Therapeutic Applications
Non-Coding RNA 2019, 5(2), 35; https://doi.org/10.3390/ncrna5020035 - 24 Apr 2019
Cited by 4
Abstract
The central nervous system can respond to threat via the induction of an inflammatory response. Under normal circumstances this response is tightly controlled, however uncontrolled neuroinflammation is a hallmark of many neurological disorders. MicroRNAs are small non-coding RNA molecules that are important for [...] Read more.
The central nervous system can respond to threat via the induction of an inflammatory response. Under normal circumstances this response is tightly controlled, however uncontrolled neuroinflammation is a hallmark of many neurological disorders. MicroRNAs are small non-coding RNA molecules that are important for regulating many cellular processes. The ability of microRNAs to modulate inflammatory signaling is an area of ongoing research, which has gained much attention in recent years. MicroRNAs may either promote or restrict inflammatory signaling, and either exacerbate or ameliorate the pathological consequences of excessive neuroinflammation. The aim of this review is to summarize the mode of regulation for several important and well-studied microRNAs in the context of neuroinflammation, including miR-155, miR-146a, miR-124, miR-21 and let-7. Furthermore, the pathological consequences of miRNA deregulation during disorders that feature neuroinflammation are discussed, including Multiple Sclerosis, Alzheimer’s disease, Parkinson’s disease, Prion diseases, Japanese encephalitis, Herpes encephalitis, ischemic stroke and traumatic brain injury. There has also been considerable interest in the use of altered microRNA signatures as biomarkers for these disorders. The ability to modulate microRNA expression may even serve as the basis for future therapeutic strategies to help treat pathological neuroinflammation. Full article
(This article belongs to the Special Issue Non-Coding RNA and the Immune System)
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Open AccessFeature PaperReview
Long Non-Coding RNAs and the Innate Immune Response
Non-Coding RNA 2019, 5(2), 34; https://doi.org/10.3390/ncrna5020034 - 19 Apr 2019
Cited by 2
Abstract
Innate immunity provides the initial defence against infection and it is now clear that long non-coding RNAs (lncRNAs) are important regulators of this response. Following activation of the innate response, we commonly see rapid induction of these lncRNAs and this is often mediated [...] Read more.
Innate immunity provides the initial defence against infection and it is now clear that long non-coding RNAs (lncRNAs) are important regulators of this response. Following activation of the innate response, we commonly see rapid induction of these lncRNAs and this is often mediated via the pro-inflammatory transcription factor, nuclear factor-κB (NF-κB). Knockdown studies have shown that lncRNAs tend to act in trans to regulate the expression of multiple inflammatory mediators and other responses. Mechanistically, many lncRNAs have demonstrated acting through heterogeneous nuclear ribonucleoproteins, complexes that are implicated chromatin re-modelling, transcription process and translation. In addition, these lncRNAs have also been shown to interact with multiple other proteins involved in the regulation of chromatin re-modelling, as well as those proteins involved in intracellular immune signalling, which include NF-κB. In this review, we will describe the evidence that supports this emerging role of lncRNA in the innate immune response. Full article
(This article belongs to the Special Issue Non-Coding RNA and the Immune System)
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Open AccessFeature PaperReview
Crosstalk Between Mammalian Antiviral Pathways
Non-Coding RNA 2019, 5(1), 29; https://doi.org/10.3390/ncrna5010029 - 22 Mar 2019
Abstract
As part of their innate immune response against viral infections, mammals activate the expression of type I interferons to prevent viral replication and dissemination. An antiviral RNAi-based response can be also activated in mammals, suggesting that several mechanisms can co-occur in the same [...] Read more.
As part of their innate immune response against viral infections, mammals activate the expression of type I interferons to prevent viral replication and dissemination. An antiviral RNAi-based response can be also activated in mammals, suggesting that several mechanisms can co-occur in the same cell and that these pathways must interact to enable the best antiviral response. Here, we will review how the classical type I interferon response and the recently described antiviral RNAi pathways interact in mammalian cells. Specifically, we will uncover how the small RNA biogenesis pathway, composed by the nucleases Drosha and Dicer can act as direct antiviral factors, and how the type-I interferon response regulates the function of these. We will also describe how the factors involved in small RNA biogenesis and specific small RNAs impact the activation of the type I interferon response and antiviral activity. With this, we aim to expose the complex and intricate network of interactions between the different antiviral pathways in mammals. Full article
(This article belongs to the Special Issue Non-Coding RNA and the Immune System)
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