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Innate Immune Cell Effector Responses
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Innate Immune Cell Effector Responses

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: closed (15 December 2022) | Viewed by 24125

Special Issue Editor

Dr. James L. Stafford

E-Mail Website
Guest Editor
Department of Biological Sciences, University of Alberta, Edmonton, AB, Canada
Interests: comparative immunology; immunoregulatory receptor-types; innate immunity; inflammation; intracellular signaling; macrophages; phagocytosis; teleost
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are soliciting primary research articles and reviews focused on the activation, control, and potency of innate immune cell effector responses initiated by vertebrate leukocytes. We welcome all contributions in this area in hope of generating a Special Issue with a broad overview of immune cell-based induction of potent antimicrobial responses required for protection from the enormous diversity of microbial pathogens. Articles covering a range of topics will be considered, including pathogen surveillance, immunoregulatory-mediated control of effector responses, innate intracellular signaling pathways, and effector response mechanisms. We also encourage articles dealing with innate immune cell effector responses from a broad range of animals and humans.

Dr. James L. Stafford
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 submissions that pass pre-check are 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
  • antimicrobial responses
  • vertebrates
  • intracellular signaling
  • phagocytosis
  • cytokine secretion
  • degranulation
  • NETosis
  • reactive nitrogen species
  • oxidative burst
  • pattern recognition receptors

Published Papers (6 papers)

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Research

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10 pages, 2870 KiB  
Article
The EphA1 and EphA2 Signaling Modulates the Epithelial Permeability in Human Sinonasal Epithelial Cells and the Rhinovirus Infection Induces Epithelial Barrier Dysfunction via EphA2 Receptor Signaling
by Jae Min Shin, Moon Soo Han, Jae Hyung Park, Seung Hyeok Lee, Tae Hoon Kim and Sang Hag Lee
Int. J. Mol. Sci. 2023, 24(4), 3629; https://doi.org/10.3390/ijms24043629 - 11 Feb 2023
Cited by 1 | Viewed by 1338
Abstract
Deficiencies in epithelial barrier integrity are involved in the pathogenesis of chronic rhinosinusitis (CRS). This study aimed to investigate the role of ephrinA1/ephA2 signaling on sinonasal epithelial permeability and rhinovirus-induced epithelial permeability. This role in the process of epithelial permeability was evaluated by [...] Read more.
Deficiencies in epithelial barrier integrity are involved in the pathogenesis of chronic rhinosinusitis (CRS). This study aimed to investigate the role of ephrinA1/ephA2 signaling on sinonasal epithelial permeability and rhinovirus-induced epithelial permeability. This role in the process of epithelial permeability was evaluated by stimulating ephA2 with ephrinA1 and inactivating ephA2 with ephA2 siRNA or inhibitor in cells exposed to rhinovirus infection. EphrinA1 treatment increased epithelial permeability, which was associated with decreased expression of ZO-1, ZO-2, and occludin. These effects of ephrinA1 were attenuated by blocking the action of ephA2 with ephA2 siRNA or inhibitor. Furthermore, rhinovirus infection upregulated the expression levels of ephrinA1 and ephA2, increasing epithelial permeability, which was suppressed in ephA2-deficient cells. These results suggest a novel role of ephrinA1/ephA2 signaling in epithelial barrier integrity in the sinonasal epithelium, suggesting their participation in rhinovirus-induced epithelial dysfunction. Full article
(This article belongs to the Special Issue Innate Immune Cell Effector Responses)
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14 pages, 2664 KiB  
Article
Canine Circovirus Suppresses the Type I Interferon Response and Protein Expression but Promotes CPV-2 Replication
by Xiangqi Hao, Yanchao Li, Hui Chen, Bo Chen, Ruohan Liu, Yidan Wu, Xiangyu Xiao, Pei Zhou and Shoujun Li
Int. J. Mol. Sci. 2022, 23(12), 6382; https://doi.org/10.3390/ijms23126382 - 07 Jun 2022
Cited by 8 | Viewed by 2588
Abstract
Canine circovirus (CanineCV) is an emerging virus in canines. Since the first strain of CanineCV was reported in 2012, CanineCV infection has shown a trend toward becoming a global epidemic. CanineCV infection often occurs with coinfection with other pathogens that may aggravate the [...] Read more.
Canine circovirus (CanineCV) is an emerging virus in canines. Since the first strain of CanineCV was reported in 2012, CanineCV infection has shown a trend toward becoming a global epidemic. CanineCV infection often occurs with coinfection with other pathogens that may aggravate the symptoms of disease in affected dogs. Currently, CanineCV has not been successfully isolated by laboratories, resulting in a lack of clarity regarding its physicochemical properties, replication process, and pathogenic characteristics. To address this knowledge gap, the following results were obtained in this study. First, a CanineCV strain was rescued in F81 cells using infectious clone plasmids. Second, the Rep protein produced by the viral packaging rescue process was found to be associated with cytopathic effects. Additionally, the Rep protein and CanineCV inhibited the activation of the type I interferon (IFN-I) promoter, blocking subsequent expression of interferon-stimulated genes (ISGs). Furthermore, Rep was found to broadly inhibit host protein expression. We speculate that in CanineCV and canine parvovirus type 2 (CPV-2) coinfection cases, CanineCV promotes CPV-2 replication by inducing immunosuppression, which may increase the severity of clinical symptoms. Full article
(This article belongs to the Special Issue Innate Immune Cell Effector Responses)
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18 pages, 1716 KiB  
Article
Modulation of Inflammatory Cytokine Production in Human Monocytes by cGMP and IRAK3
by Trang H. Nguyen, Anna Axell, Ilona Turek, Bree Wright, Terri Meehan-Andrews and Helen R. Irving
Int. J. Mol. Sci. 2022, 23(5), 2552; https://doi.org/10.3390/ijms23052552 - 25 Feb 2022
Cited by 10 | Viewed by 3246
Abstract
Interleukin-1 receptor-associated kinase-3 (IRAK3) is a critical checkpoint molecule of inflammatory responses in the innate immune system. The pseudokinase domain of IRAK3 contains a guanylate cyclase (GC) centre that generates small amounts of cyclic guanosine monophosphate (cGMP) associated with IRAK3 functions in inflammation. [...] Read more.
Interleukin-1 receptor-associated kinase-3 (IRAK3) is a critical checkpoint molecule of inflammatory responses in the innate immune system. The pseudokinase domain of IRAK3 contains a guanylate cyclase (GC) centre that generates small amounts of cyclic guanosine monophosphate (cGMP) associated with IRAK3 functions in inflammation. However, the mechanisms of IRAK3 actions are poorly understood. The effects of low cGMP levels on inflammation are unknown, therefore a dose–response effect of cGMP on inflammatory markers was assessed in THP-1 monocytes challenged with lipopolysaccharide (LPS). Sub-nanomolar concentrations of membrane permeable 8-Br-cGMP reduced LPS-induced NFκB activity, IL-6 and TNF-α cytokine levels. Pharmacologically upregulating cellular cGMP levels using a nitric oxide donor reduced cytokine secretion. Downregulating cellular cGMP using a soluble GC inhibitor increased cytokine levels. Knocking down IRAK3 in THP-1 cells revealed that unlike the wild type cells, 8-Br-cGMP did not suppress inflammatory responses. Complementation of IRAK3 knockdown cells with wild type IRAK3 suppressed cytokine production while complementation with an IRAK3 mutant at GC centre only partially restored this function. Together these findings indicate low levels of cGMP form a critical component in suppressing cytokine production and in mediating IRAK3 action, and this may be via a cGMP enriched nanodomain formed by IRAK3 itself. Full article
(This article belongs to the Special Issue Innate Immune Cell Effector Responses)
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Review

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13 pages, 1286 KiB  
Review
How the Innate Immune DNA Sensing cGAS-STING Pathway Is Involved in Apoptosis
by Wanglong Zheng, Anjing Liu, Nengwen Xia, Nanhua Chen, François Meurens and Jianzhong Zhu
Int. J. Mol. Sci. 2023, 24(3), 3029; https://doi.org/10.3390/ijms24033029 - 03 Feb 2023
Cited by 13 | Viewed by 4331
Abstract
The cGAS–STING signaling axis can be activated by cytosolic DNA, including both non-self DNA and self DNA. This axis is used by the innate immune system to monitor invading pathogens and/or damage. Increasing evidence has suggested that the cGAS-STING pathway not only facilitates [...] Read more.
The cGAS–STING signaling axis can be activated by cytosolic DNA, including both non-self DNA and self DNA. This axis is used by the innate immune system to monitor invading pathogens and/or damage. Increasing evidence has suggested that the cGAS-STING pathway not only facilitates inflammatory responses and the production of type I interferons (IFN), but also activates other cellular processes, such as apoptosis. Recently, many studies have focused on analyzing the mechanisms of apoptosis induced by the cGAS-STING pathway and their consequences. This review gives a detailed account of the interplay between the cGAS-STING pathway and apoptosis. The cGAS-STING pathway can induce apoptosis through ER stress, NLRP3, NF-κB, IRF3, and IFN signals. Conversely, apoptosis can feed back to regulate the cGAS-STING pathway, suppressing it via the activation of caspases or promoting it via mitochondrial DNA (mtDNA) release. Apoptosis mediated by the cGAS-STING pathway plays crucial roles in balancing innate immune responses, resisting infections, and limiting tumor growth. Full article
(This article belongs to the Special Issue Innate Immune Cell Effector Responses)
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35 pages, 3523 KiB  
Review
The Expanding Role of Extracellular Traps in Inflammation and Autoimmunity: The New Players in Casting Dark Webs
by Stephanie U-Shane Huang and Kim Maree O’Sullivan
Int. J. Mol. Sci. 2022, 23(7), 3793; https://doi.org/10.3390/ijms23073793 - 30 Mar 2022
Cited by 26 | Viewed by 5389
Abstract
The first description of a new form of neutrophil cell death distinct from that of apoptosis or necrosis was discovered in 2004 and coined neutrophil extracellular traps “(NETs)” or “NETosis”. Different stimuli for NET formation, and pathways that drive neutrophils to commit to [...] Read more.
The first description of a new form of neutrophil cell death distinct from that of apoptosis or necrosis was discovered in 2004 and coined neutrophil extracellular traps “(NETs)” or “NETosis”. Different stimuli for NET formation, and pathways that drive neutrophils to commit to NETosis have been elucidated in the years that followed. Critical enzymes required for NET formation have been discovered and targeted therapeutically. NET formation is no longer restricted to neutrophils but has been discovered in other innate cells: macrophages/monocytes, mast Cells, basophils, dendritic cells, and eosinophils. Furthermore, extracellular DNA can also be extruded from both B and T cells. It has become clear that although this mechanism is thought to enhance host defense by ensnaring bacteria within large webs of DNA to increase bactericidal killing capacity, it is also injurious to innocent bystander tissue. Proteases and enzymes released from extracellular traps (ETs), injure epithelial and endothelial cells perpetuating inflammation. In the context of autoimmunity, ETs release over 70 well-known autoantigens. ETs are associated with pathology in multiple diseases: lung diseases, vasculitis, autoimmune kidney diseases, atherosclerosis, rheumatoid arthritis, cancer, and psoriasis. Defining these pathways that drive ET release will provide insight into mechanisms of pathological insult and provide potential therapeutic targets. Full article
(This article belongs to the Special Issue Innate Immune Cell Effector Responses)
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14 pages, 2502 KiB  
Review
How the Innate Immune DNA Sensing cGAS–STING Pathway Is Involved in Autophagy
by Wanglong Zheng, Nengwen Xia, Jiajia Zhang, Nanhua Chen, François Meurens, Zongping Liu and Jianzhong Zhu
Int. J. Mol. Sci. 2021, 22(24), 13232; https://doi.org/10.3390/ijms222413232 - 08 Dec 2021
Cited by 14 | Viewed by 6653
Abstract
The cGAS–STING pathway is a key component of the innate immune system and exerts crucial roles in the detection of cytosolic DNA and invading pathogens. Accumulating evidence suggests that the intrinsic cGAS–STING pathway not only facilitates the production of type I interferons (IFN-I) [...] Read more.
The cGAS–STING pathway is a key component of the innate immune system and exerts crucial roles in the detection of cytosolic DNA and invading pathogens. Accumulating evidence suggests that the intrinsic cGAS–STING pathway not only facilitates the production of type I interferons (IFN-I) and inflammatory responses but also triggers autophagy. Autophagy is a homeostatic process that exerts multiple effects on innate immunity. However, systematic evidence linking the cGAS–STING pathway and autophagy is still lacking. Therefore, one goal of this review is to summarize the known mechanisms of autophagy induced by the cGAS–STING pathway and their consequences. The cGAS–STING pathway can trigger canonical autophagy through liquid-phase separation of the cGAS–DNA complex, interaction of cGAS and Beclin-1, and STING-triggered ER stress–mTOR signaling. Furthermore, both cGAS and STING can induce non-canonical autophagy via LC3-interacting regions and binding with LC3. Subsequently, autophagy induced by the cGAS–STING pathway plays crucial roles in balancing innate immune responses, maintaining intracellular environmental homeostasis, alleviating liver injury, and limiting tumor growth and transformation. Full article
(This article belongs to the Special Issue Innate Immune Cell Effector Responses)
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