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Special Issue "DNA or RNA-Mediated Innate Immune Response"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 15 June 2021.

Special Issue Editors

Dr. Tomozumi Imamichi
Website
Guest Editor
Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA
Interests: HIV, viral fitness, innat immunity, non-coding RNA, autophage, Interleukin-27, Interferon lambda-1, Reactive Oxygen Specises Webpage: https://david.ncifcrf.gov
Dr. Hongyan Sui

Guest Editor
Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA
Interests: all forms of RNA or DNA, including siRNA, miRNA, long non-coding RNA, DNA virus pathengen-induced Interferons and inflammatory cytokines, especially the mechanism of type III interferon inducing pathway

Special Issue Information

Dear Colleagues,

Innate immunity is the first line of defense and relies on germline-encoded pattern recognition receptors (PRRs) that primarily recognize conserved microbial molecules termed pathogen-associated molecular patterns (PAMPs). It has been known for over a decade that DNA or RNA, the most recognizable unit of life, is a potent trigger of induction interferons and proinflammatory cytokines in cells. Nucleic acids and their derivatives are one of the most important groups of PAMPs, particularly in the innate immune response against viruses. Research in the last decade has led to the identification and characterization of an increasing number of extracellular and intracellular PRRs. Two main classes of PRRs have been described in mammalian cells: membrane-bound receptors, such as Toll-like receptors (TLRs) and C-type lectin receptors (CLRs), and cytoplasmic sensors, including NOD-like receptors (NLRs), pyrin and HIN domain-containing (PYHIN) family members, RIG-I-like receptors (RLRs), and an increasing range of cytosolic nucleic acid sensors. However, how a new pathogen is recognized and how innate immune responses are initiated in different tissues or cells remain case-by-case questions. In turn, viruses have strategies to escape from the innate immure response by suppressing the signal pathway involved in the immune responses.

This Special Issue “DNA or RNA-Mediated Innate Immune Response” will cover a selection of original research articles, short communications, and current review articles in all areas of DNA or RNA-mediated innate immunity.

Dr. Tomozumi Imamichi
Dr. Hongyan Sui
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • innate immunity
  • interferons
  • inflammatory cytokines
  • pattern recognition receptors (PRRs)
  • pathogen-associated molecular patterns (PAMPs)

Published Papers (5 papers)

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Research

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Open AccessArticle
MicroRNA Profiles in Monocyte-Derived Macrophages Generated by Interleukin-27 and Human Serum: Identification of a Novel HIV-Inhibiting and Autophagy-Inducing MicroRNA
Int. J. Mol. Sci. 2021, 22(3), 1290; https://doi.org/10.3390/ijms22031290 - 28 Jan 2021
Abstract
Interleukin-27 (IL-27) is a pleiotropic cytokine that influences the innate and adaptive immune systems. It inhibits viral infection and regulates the expression of microRNAs (miRNAs). We recently reported that macrophages differentiated from human primary monocytes in the presence of IL-27 and human AB [...] Read more.
Interleukin-27 (IL-27) is a pleiotropic cytokine that influences the innate and adaptive immune systems. It inhibits viral infection and regulates the expression of microRNAs (miRNAs). We recently reported that macrophages differentiated from human primary monocytes in the presence of IL-27 and human AB serum resisted human immunodeficiency virus (HIV) infection and showed significant autophagy induction. In the current study, the miRNA profiles in these cells were investigated, especially focusing on the identification of novel miRNAs regulated by IL-27-treatment. The miRNA sequencing analysis detected 38 novel miRNAs. Real-time reverse transcription polymerase chain reaction (RT-PCR) analysis confirmed that IL-27 differentially regulated the expression of 16 of the 38 miRNAs. Overexpression of the synthesized miRNA mimics by transfection revealed that miRAB40 had potent HIV-inhibiting and autophagy-inducing properties. B18R, an interferon (IFN)-neutralization protein, partially suppressed both activities, indicating that the two functions were induced via IFN-dependent and -independent pathways. Although the target mRNA(s) of miRAB40 involving in the induction of both functions was unable to identify in this study, the discovery of miRAB40, a potential HIV-inhibiting and autophagy inducing miRNA, may provide novel insights into the miRNA (small none-coding RNA)-mediated regulation of HIV inhibition and autophagy induction as an innate immune response. Full article
(This article belongs to the Special Issue DNA or RNA-Mediated Innate Immune Response)
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Open AccessArticle
The Drosophila miR-959–962 Cluster Members Repress Toll Signaling to Regulate Antibacterial Defense during Bacterial Infection
Int. J. Mol. Sci. 2021, 22(2), 886; https://doi.org/10.3390/ijms22020886 - 17 Jan 2021
Abstract
MicroRNAs (miRNAs) are a class of ~22 nt non-coding RNA molecules in metazoans capable of down-regulating target gene expression by binding to the complementary sites in the mRNA transcripts. Many individual miRNAs are implicated in a broad range of biological pathways, but functional [...] Read more.
MicroRNAs (miRNAs) are a class of ~22 nt non-coding RNA molecules in metazoans capable of down-regulating target gene expression by binding to the complementary sites in the mRNA transcripts. Many individual miRNAs are implicated in a broad range of biological pathways, but functional characterization of miRNA clusters in concert is limited. Here, we report that miR-959–962 cluster (miR-959/960/961/962) can weaken Drosophila immune response to bacterial infection evidenced by the reduced expression of antimicrobial peptide Drosomycin (Drs) and short survival within 24 h upon infection. Each of the four miRNA members is confirmed to contribute to the reduced Drs expression and survival rate of Drosophila. Mechanically, RT-qPCR and Dual-luciferase reporter assay verify that tube and dorsal (dl) mRNAs, key components of Toll pathway, can simultaneously be targeted by miR-959 and miR-960, miR-961, and miR-962, respectively. Furthermore, miR-962 can even directly target to the 3′ untranslated region (UTR) of Toll. In addition, the dynamic expression pattern analysis in wild-type flies reveals that four miRNA members play important functions in Drosophila immune homeostasis restoration at the late stage of Micrococcus luteus (M. luteus) infection. Taken together, our results identify four miRNA members from miR-959–962 cluster as novel suppressors of Toll signaling and enrich the repertoire of immune-modulating miRNA in Drosophila. Full article
(This article belongs to the Special Issue DNA or RNA-Mediated Innate Immune Response)
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Open AccessArticle
Interferon-Mediated Long Non-Coding RNA Response in Macrophages in the Context of HIV
Int. J. Mol. Sci. 2020, 21(20), 7741; https://doi.org/10.3390/ijms21207741 - 19 Oct 2020
Abstract
Interferons play a critical role in the innate immune response against a variety of pathogens, such as HIV-1. Recent studies have shown that long non-coding genes are part of a reciprocal feedforward/feedback relationship with interferon expression. They presumably contribute to the cell type [...] Read more.
Interferons play a critical role in the innate immune response against a variety of pathogens, such as HIV-1. Recent studies have shown that long non-coding genes are part of a reciprocal feedforward/feedback relationship with interferon expression. They presumably contribute to the cell type specificity of the interferon response, such as the phenotypic and functional transition of macrophages throughout the immune response. However, no comprehensive understanding exists today about the IFN–lncRNA interplay in macrophages, also a sanctuary for latent HIV-1. Therefore, we completed a poly-A+ RNAseq analysis on monocyte-derived macrophages (MDMs) treated with members of all three types of IFNs (IFN-α, IFN-ε, IFN-γ or IFN-λ) and on macrophages infected with HIV-1, revealing an extensive non-coding IFN and/or HIV-1 response. Moreover, co-expression correlation with mRNAs was used to identify important (long) non-coding hub genes within IFN- or HIV-1-associated gene clusters. This study identified and prioritized IFN related hub lncRNAs for further functional validation. Full article
(This article belongs to the Special Issue DNA or RNA-Mediated Innate Immune Response)
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Review

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Open AccessReview
Role of Post-Translational Modifications of cGAS in Innate Immunity
Int. J. Mol. Sci. 2020, 21(21), 7842; https://doi.org/10.3390/ijms21217842 - 22 Oct 2020
Cited by 1
Abstract
Cyclic GMP–AMP synthase (cGAS) is the synthase that generates the second messenger cyclic GMP–AMP (cGAMP) upon DNA binding. cGAS was first discovered as the cytosolic DNA sensor that detects DNA exposed in the cytoplasm either from pathogens or cellular damage. Activated cGAS instigates [...] Read more.
Cyclic GMP–AMP synthase (cGAS) is the synthase that generates the second messenger cyclic GMP–AMP (cGAMP) upon DNA binding. cGAS was first discovered as the cytosolic DNA sensor that detects DNA exposed in the cytoplasm either from pathogens or cellular damage. Activated cGAS instigates the signaling cascades to activate type I interferon (IFN) expression, critical for host defense and autoimmune diseases. In addition, cGAS plays a role in senescence, DNA repair, apoptosis, and tumorigenesis. Recently, various post-translational modifications (PTMs) of cGAS have been reported, such as phosphorylation, ubiquitination, acetylation, glutamylation, and sumoylation. These PTMs profoundly affect cGAS functions. Thus, here we review the recent reported PTMs of cGAS and how these PTMs regulate cGAS enzymatic activity, DNA binding, and protein stability, and discuss the potential future directions. Full article
(This article belongs to the Special Issue DNA or RNA-Mediated Innate Immune Response)
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Open AccessReview
A Role of Intracellular Toll-Like Receptors (3, 7, and 9) in Response to Mycobacterium tuberculosis and Co-Infection with HIV
Int. J. Mol. Sci. 2020, 21(17), 6148; https://doi.org/10.3390/ijms21176148 - 26 Aug 2020
Abstract
Mycobacterium tuberculosis (Mtb) is a highly infectious acid-fast bacillus and is known to cause tuberculosis (TB) in humans. It is a leading cause of death from a sole infectious agent, with an estimated 1.5 million deaths yearly worldwide, and up to one third [...] Read more.
Mycobacterium tuberculosis (Mtb) is a highly infectious acid-fast bacillus and is known to cause tuberculosis (TB) in humans. It is a leading cause of death from a sole infectious agent, with an estimated 1.5 million deaths yearly worldwide, and up to one third of the world’s population has been infected with TB. The virulence and susceptibility of Mtb are further amplified in the presence of Human Immunodeficiency Virus (HIV). Coinfection with Mtb and HIV forms a lethal combination. Previous studies had demonstrated the synergistic effects of Mtb and HIV, with one disease accelerating the disease progression of the other through multiple mechanisms, including the modulation of the immune response to these two pathogens. The response of the endosomal pattern recognition receptors to these two pathogens, specifically toll-like receptors (TLR)-3, -7, and -9, has not been elucidated, with some studies producing mixed results. This article seeks to review the roles of TLR-3, -7, and -9 in response to Mtb infection, as well as Mtb-HIV-coinfection via Toll-interleukin 1 receptor (TIR) domain-containing adaptor inducing INF-β (TRIF)-dependent and myeloid differentiation factor 88 (MyD88)-dependent pathways. Full article
(This article belongs to the Special Issue DNA or RNA-Mediated Innate Immune Response)
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