Special Issue "NF-kappa B in Inflammation and Immunity"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: 1 September 2020.

Special Issue Editor

Prof. Eijiro Jimi
Website
Guest Editor
Oral health/Brain health/Total health Center, Faculty of Dental Science, Kyushu University, Fukuoka, Japan
Interests: NF-κB; inflammatory disease; immune respsonse; cancer

Special Issue Information

Dear Colleagues,

Since nuclear factor-κB (NF-κB) was originally identified as a transcriptional factor that bound to the enhancer region of immunoglobulin κ light-chain promoter in B cells. It was thought that NF-κB plays crucial roles in B cell development; however, as research progressed, it became clear that NF-κB was involved in the expression of a wide variety of genes related to inflammation, immune responses, cell proliferation, tumorigenesis, and survival. The NF-κB family consists of five members, p65 (RelA), c-Rel, RelB, NF-κB1 (p105/p50), and NF-κB2 (p100/p52). NF-κB family member is evolutionarily conserved and ubiquitously expressed in mammals. The activation of NF-κB signaling is strictly regulated. Generally, NF-κB predominantly exists in cytoplasm in an unstimulated state. In response to a variety of stimuli, NF-κB translocates into the nucleus and then binds to the promoter region of target genes. Several molecules regulating the NF-κB signaling pathway have also been identified, whereas dysregulation of the NF-κB signaling pathway, due to losing or gaining the function of the NF-κB family member and regulating molecules, leads to several diseases, such as inflammation, cancer, or metabolic disorders. This Special Issue of Cells covers much of what is known or new aspects about the NF-κB signaling pathway and its function. We believe that the reviews shown in this Issue will be of interest to a broad group of scientists who are involved in not only molecular and cell biology but also translational research.

Prof. Eijiro Jimi
Guest Editor

Manuscript Submission Information

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Keywords

  • NF-κB
  • Inflammatory disease
  • Immune response
  • Cancer

Published Papers (4 papers)

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Research

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Open AccessArticle
Pro-Inflammatory Signaling Upregulates a Neurotoxic Conotoxin-Like Protein Encrypted Within Human Endogenous Retrovirus-K
Cells 2020, 9(7), 1584; https://doi.org/10.3390/cells9071584 (registering DOI) - 30 Jun 2020
Abstract
Motor neuron degeneration and spinal cord demyelination are hallmark pathological events in Amyotrophic Lateral Sclerosis (ALS). Endogenous retrovirus-K (ERVK) expression has an established association with ALS neuropathology, with murine modeling pointing to a role for the ERVK envelope (env) gene in [...] Read more.
Motor neuron degeneration and spinal cord demyelination are hallmark pathological events in Amyotrophic Lateral Sclerosis (ALS). Endogenous retrovirus-K (ERVK) expression has an established association with ALS neuropathology, with murine modeling pointing to a role for the ERVK envelope (env) gene in disease processes. Here, we describe a novel viral protein cryptically encoded within the ERVK env transcript, which resembles two distinct cysteine-rich neurotoxic proteins: conotoxin proteins found in marine snails and the Human Immunodeficiency Virus (HIV) Tat protein. Consistent with Nuclear factor-kappa B (NF-κB)-induced retrotransposon expression, the ERVK conotoxin-like protein (CTXLP) is induced by inflammatory signaling. CTXLP is found in the nucleus, impacting innate immune gene expression and NF-κB p65 activity. Using human autopsy specimens from patients with ALS, we further showcase CTXLP expression in degenerating motor cortex and spinal cord tissues, concomitant with inflammation linked pathways, including enhancement of necroptosis marker mixed lineage kinase domain-like (MLKL) protein and oligodendrocyte maturation/myelination inhibitor Nogo-A. These findings identify CTXLP as a novel ERVK protein product, which may act as an effector in ALS neuropathology. Full article
(This article belongs to the Special Issue NF-kappa B in Inflammation and Immunity)
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Review

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Open AccessFeature PaperReview
Cell-Type Targeted NF-kappaB Inhibition for the Treatment of Inflammatory Diseases
Cells 2020, 9(7), 1627; https://doi.org/10.3390/cells9071627 - 06 Jul 2020
Abstract
Deregulated NF-k activation is not only involved in cancer but also contributes to the pathogenesis of chronic inflammatory diseases like rheumatoid arthritis (RA) and multiple sclerosis (MS). Ideally, therapeutic NF-KappaB inhibition should only take place in those cell types that are involved in [...] Read more.
Deregulated NF-k activation is not only involved in cancer but also contributes to the pathogenesis of chronic inflammatory diseases like rheumatoid arthritis (RA) and multiple sclerosis (MS). Ideally, therapeutic NF-KappaB inhibition should only take place in those cell types that are involved in disease pathogenesis to maintain physiological cell functions in all other cells. In contrast, unselective NF-kappaB inhibition in all cells results in multiple adverse effects, a major hindrance in drug development. Hitherto, various substances exist to inhibit different steps of NF-kappaB signaling. However, powerful tools for cell-type specific NF-kappaB inhibition are not yet established. Here, we review the role of NF-kappaB in inflammatory diseases, current strategies for drug delivery and NF-kappaB inhibition and point out the “sneaking ligand” approach. Sneaking ligand fusion proteins (SLFPs) are recombinant proteins with modular architecture consisting of three domains. The prototype SLC1 binds specifically to the activated endothelium and blocks canonical NF-kappaB activation. In vivo, SLC1 attenuated clinical and histological signs of experimental arthritides. The SLFP architecture allows an easy exchange of binding and effector domains and represents an attractive approach to study disease-relevant biological targets in a broad range of diseases. In vivo, SLFP treatment might increase therapeutic efficacy while minimizing adverse effects. Full article
(This article belongs to the Special Issue NF-kappa B in Inflammation and Immunity)
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Open AccessReview
NF-κB and tPA Signaling in Kidney and Other Diseases
Cells 2020, 9(6), 1348; https://doi.org/10.3390/cells9061348 - 29 May 2020
Abstract
The activation of the nuclear factor-κB (NF-κB) pathway plays a central role in the initiation and progression of inflammation, which contributes to the pathogenesis and progression of various human diseases including kidney, brain, and other diseases. Tissue plasminogen activator (tPA), a serine protease [...] Read more.
The activation of the nuclear factor-κB (NF-κB) pathway plays a central role in the initiation and progression of inflammation, which contributes to the pathogenesis and progression of various human diseases including kidney, brain, and other diseases. Tissue plasminogen activator (tPA), a serine protease regulating homeostasis of blood coagulation, fibrinolysis, and matrix degradation, has been shown to act as a cytokine to trigger profound receptor-mediated intracellular events, modulate the NF-κB pathway, and mediate organ dysfunction and injury. In this review, we focus on the current understanding of NF-κB and tPA signaling in the development and progression of kidney disease. Their roles in the nervous and cardiovascular system are also briefly discussed. Full article
(This article belongs to the Special Issue NF-kappa B in Inflammation and Immunity)
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Open AccessFeature PaperReview
The Role of NF-κB in Physiological Bone Development and Inflammatory Bone Diseases: Is NF-κB Inhibition “Killing Two Birds with One Stone”?
Cells 2019, 8(12), 1636; https://doi.org/10.3390/cells8121636 - 14 Dec 2019
Cited by 2
Abstract
Nuclear factor-κB (NF-κB) is a transcription factor that regulates the expression of various genes involved in inflammation and the immune response. The activation of NF-κB occurs via two pathways: inflammatory cytokines, such as TNF-α and IL-1β, activate the “classical pathway”, and cytokines involved [...] Read more.
Nuclear factor-κB (NF-κB) is a transcription factor that regulates the expression of various genes involved in inflammation and the immune response. The activation of NF-κB occurs via two pathways: inflammatory cytokines, such as TNF-α and IL-1β, activate the “classical pathway”, and cytokines involved in lymph node formation, such as CD40L, activate the “alternative pathway”. NF-κB1 (p50) and NF-κB2 (p52) double-knockout mice exhibited severe osteopetrosis due to the total lack of osteoclasts, suggesting that NF-κB activation is required for osteoclast differentiation. These results indicate that NF-κB may be a therapeutic target for inflammatory bone diseases, such as rheumatoid arthritis and periodontal disease. On the other hand, mice that express the dominant negative form of IκB kinase (IKK)-β specifically in osteoblasts exhibited increased bone mass, but there was no change in osteoclast numbers. Therefore, inhibition of NF-κB is thought to promote bone formation. Taken together, the inhibition of NF-κB leads to “killing two birds with one stone”: it suppresses bone resorption and promotes bone formation. This review describes the role of NF-κB in physiological bone metabolism, pathologic bone destruction, and bone regeneration. Full article
(This article belongs to the Special Issue NF-kappa B in Inflammation and Immunity)
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