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Cells
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Innate Immune System in Immune-Mediated Inflammatory Diseases (IMIDs)
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Innate Immune System in Immune-Mediated Inflammatory Diseases (IMIDs)

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

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 20784

Special Issue Editors

Dr. Javier Conde Aranda

E-Mail Website
Guest Editor
Molecular and Cellular Gastroenterology, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain
Interests: inflammation; immune-mediated diseases; inflammatory bowel disease; colorectal cancer; resolution of inflammation
Special Issues, Collections and Topics in MDPI journals
Dr. Samuel García Pérez

E-Mail Website
Guest Editor
Rheumatology & Immune-Mediated Diseases (IRIDIS) group, Galicia Sur Health Research Institute (IIS Galicia Sur), Vigo, Spain
Interests: rheumatic and musculoskeletal diseases (RMDs); rheumatoid arthritis; psoriatic arthritis; systemic lupus erythematosus; systemic sclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Immune-mediated inflammatory diseases (IMIDs) are a diverse group of disorders characterized by the dysregulation of immune response, which results in chronic inflammation in different tissues and systems. Among these, there are pathologies directly related to an aberrant immune response, such as rheumatoid arthritis, inflammatory bowel disease, and asthma. However, IMIDs include other conditions in which the immune system is not the primary cause of the disease—e.g., cancer or infectious diseases.

Typically, the adaptive immune system has been considered the most relevant player in the development of many IMIDs. However, at present it is generally accepted that the innate immune system is equally important for the regulation and maintenance of tissue homeostasis. In fact, alterations in the mechanisms that regulate the innate immune response are responsible for an uncontrolled and exacerbated inflammatory response in intestinal tissue, among others. For this reason, more research is needed to understand the specific role played by the innate immune system during the onset and progression of IMIDs and for the development of new therapeutic approaches for these group of malignancies.

This Special Issue will include basic and translational original articles focused on aspects of innate immune responses related to IMIDs. Potential topics include autoimmune diseases, chronic inflammatory diseases, infectious diseases, immunodeficiencies, immunoproliferative disorders, or cancer.

Dr. Javier Aranda
Dr. Samuel Pérez
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 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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • rheumatoid arthritis
  • inflammatory bowel disease
  • psoriasis
  • psoriatic arthritis
  • vasculitis
  • Sjögren syndrome
  • ankilosing spondylitis
  • Behcet's disease
  • asthma
  • systemic lupus erythematosus
  • systemic sclerosis

Published Papers (5 papers)

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Research

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21 pages, 7342 KiB  
Article
Osthole Inhibits Expression of Genes Associated with Toll-like Receptor 2 Signaling Pathway in an Organotypic 3D Skin Model of Human Epidermis with Atopic Dermatitis
by Natalia Karolina Kordulewska, Justyna Topa, Robert Stryiński and Beata Jarmołowska
Cells 2022, 11(1), 88; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11010088 - 28 Dec 2021
Cited by 5 | Viewed by 3053
Abstract
The Toll-like receptor (TLR) family signature has been linked to the etiopathology of atopic dermatitis (AD), a chronic inflammatory skin disease associated with skin barrier dysfunction and immune system imbalance. We aimed to investigate whether osthole (a plant-derived compound) can inhibit the genetic [...] Read more.
The Toll-like receptor (TLR) family signature has been linked to the etiopathology of atopic dermatitis (AD), a chronic inflammatory skin disease associated with skin barrier dysfunction and immune system imbalance. We aimed to investigate whether osthole (a plant-derived compound) can inhibit the genetic profile of key genes associated with TLR2 signaling (TIRAP, MyD88, IRAK1, TRAF6, IκBα, NFκB) after stimulation with LPS or histamine in a 3D in vitro model of AD. Overexpression of the aforementioned genes may directly increase the secretion of proinflammatory cytokines (CKs) and chemokines (ChKs), which may exacerbate the symptoms of AD. Relative gene expressions were quantified by qPCR and secretion of CKs and ChKs was evaluated by ELISA assay. LPS and histamine increased the relative expression of genes related to the TLR2 pathway, and osthole successfully reduced it. In summary, our results show that osthole inhibits the expression of genes associated with the TLR signaling pathway in a skin model of AD. Moreover, the secretion of CKs and ChKs after treatment of AD with osthole in a 3D skin model in vitro suggests the potential of osthole as a novel compound for the treatment of AD. Full article
(This article belongs to the Special Issue Innate Immune System in Immune-Mediated Inflammatory Diseases (IMIDs))
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11 pages, 1876 KiB  
Article
Interleukin-26 Has Synergistic Catabolic Effects with Palmitate in Human Articular Chondrocytes via the TLR4-ERK1/2-c-Jun Signaling Pathway
by Yi-Ting Chen, Chih-Chien Wang, Chia-Pi Cheng, Feng-Cheng Liu, Chian-Her Lee, Herng-Sheng Lee and Yi-Jen Peng
Cells 2021, 10(9), 2500; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10092500 - 21 Sep 2021
Cited by 4 | Viewed by 2428
Abstract
The inflammatory cytokine interleukin-26 (IL-26) is highly expressed in the serum and synovial fluid of patients with inflammatory arthritis. The effect of IL-26 on human articular chondrocytes (HACs) remains unclear. Obesity is associated with disability of patients with rheumatoid arthritis and disease activity [...] Read more.
The inflammatory cytokine interleukin-26 (IL-26) is highly expressed in the serum and synovial fluid of patients with inflammatory arthritis. The effect of IL-26 on human articular chondrocytes (HACs) remains unclear. Obesity is associated with disability of patients with rheumatoid arthritis and disease activity in those with ankylosing spondylitis. The saturated free fatty acid palmitate with IL-1β can synergistically induce catabolic effects in HACs. The aim of this study was to evaluate the effects of IL-26 and palmitate in HACs. In this study, palmitate markedly synergizes the IL-26-induced proinflammatory effects and matrix protease, including COX-2, IL-6, and MMP-1, in HACs via the toll-like receptor 4 (TLR4)-ERK1/2-c-Jun signal transduction pathway. The synergistic catabolic effects of palmitate and IL-26 were attenuated by inhibitors of TLR4 (TAK242), ERK1/2 (U0126), or c-Jun (SP600125) in HACs and cartilage matrix. In addition, metformin, a potential inhibitor of TLR4, also decreased expression of COX-2 and IL-6 induced by co-incubation with IL-26 and palmitate. IL-26 and palmitate synergistically induced expression of inflammatory and catabolic mediators, resulting in articular cartilage matrix breakdown. The present study also revealed a possible mechanism and therapeutic targets against articular cartilage degradation by increased saturated fatty acids in patients with inflammatory arthritis. Full article
(This article belongs to the Special Issue Innate Immune System in Immune-Mediated Inflammatory Diseases (IMIDs))
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Review

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28 pages, 33351 KiB  
Review
Sympathetic Nerves and Innate Immune System in the Spleen: Implications of Impairment in HIV-1 and Relevant Models
by Denise L. Bellinger and Dianne Lorton
Cells 2022, 11(4), 673; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11040673 - 15 Feb 2022
Cited by 2 | Viewed by 3261
Abstract
The immune and sympathetic nervous systems are major targets of human, murine and simian immunodeficiency viruses (HIV-1, MAIDS, and SIV, respectively). The spleen is a major reservoir for these retroviruses, providing a sanctuary for persistent infection of myeloid cells in the white and [...] Read more.
The immune and sympathetic nervous systems are major targets of human, murine and simian immunodeficiency viruses (HIV-1, MAIDS, and SIV, respectively). The spleen is a major reservoir for these retroviruses, providing a sanctuary for persistent infection of myeloid cells in the white and red pulps. This is despite the fact that circulating HIV-1 levels remain undetectable in infected patients receiving combined antiretroviral therapy. These viruses sequester in immune organs, preventing effective cures. The spleen remains understudied in its role in HIV-1 pathogenesis, despite it hosting a quarter of the body’s lymphocytes and diverse macrophage populations targeted by HIV-1. HIV-1 infection reduces the white pulp, and induces perivascular hyalinization, vascular dysfunction, tissue infarction, and chronic inflammation characterized by activated epithelial-like macrophages. LP-BM5, the retrovirus that induces MAIDS, is a well-established model of AIDS. Immune pathology in MAIDs is similar to SIV and HIV-1 infection. As in SIV and HIV, MAIDS markedly changes splenic architecture, and causes sympathetic dysfunction, contributing to inflammation and immune dysfunction. In MAIDs, SIV, and HIV, the viruses commandeer splenic macrophages for their replication, and shift macrophages to an M2 phenotype. Additionally, in plasmacytoid dendritic cells, HIV-1 blocks sympathetic augmentation of interferon-β (IFN-β) transcription, which promotes viral replication. Here, we review viral–sympathetic interactions in innate immunity and pathophysiology in the spleen in HIV-1 and relevant models. The situation remains that research in this area is still sparse and original hypotheses proposed largely remain unanswered. Full article
(This article belongs to the Special Issue Innate Immune System in Immune-Mediated Inflammatory Diseases (IMIDs))
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20 pages, 912 KiB  
Review
Monocytes and Macrophages in Spondyloarthritis: Functional Roles and Effects of Current Therapies
by Sara Martínez-Ramos, Carlos Rafael-Vidal, José M. Pego-Reigosa and Samuel García
Cells 2022, 11(3), 515; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11030515 - 02 Feb 2022
Cited by 16 | Viewed by 3291
Abstract
Spondyloarthritis (SpA) is a family of chronic inflammatory diseases, being the most prevalent ankylosing spondylitis (AS) and psoriatic arthritis (PsA). These diseases share genetic, clinical and immunological features, such as the implication of human leukocyte antigen (HLA) class I molecule 27 (HLA-B27), the [...] Read more.
Spondyloarthritis (SpA) is a family of chronic inflammatory diseases, being the most prevalent ankylosing spondylitis (AS) and psoriatic arthritis (PsA). These diseases share genetic, clinical and immunological features, such as the implication of human leukocyte antigen (HLA) class I molecule 27 (HLA-B27), the inflammation of peripheral, spine and sacroiliac joints and the presence of extra-articular manifestations (psoriasis, anterior uveitis, enthesitis and inflammatory bowel disease). Monocytes and macrophages are essential cells of the innate immune system and are the first line of defence against external agents. In rheumatic diseases including SpA, the frequency and phenotypic and functional characteristics of both cell types are deregulated and are involved in the pathogenesis of these diseases. In fact, monocytes and macrophages play key roles in the inflammatory processes characteristics of SpA. The aim of this review is analysing the characteristics and functional roles of monocytes and macrophages in these diseases, as well as the impact of different current therapies on these cell types. Full article
(This article belongs to the Special Issue Innate Immune System in Immune-Mediated Inflammatory Diseases (IMIDs))
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23 pages, 2077 KiB  
Review
Tuning Monocytes and Macrophages for Personalized Therapy and Diagnostic Challenge in Rheumatoid Arthritis
by Leszek Roszkowski and Marzena Ciechomska
Cells 2021, 10(8), 1860; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10081860 - 22 Jul 2021
Cited by 18 | Viewed by 7616
Abstract
Monocytes/macrophages play a central role in chronic inflammatory disorders, including rheumatoid arthritis (RA). Activation of these cells results in the production of various mediators responsible for inflammation and RA pathogenesis. On the other hand, the depletion of macrophages using specific antibodies or chemical [...] Read more.
Monocytes/macrophages play a central role in chronic inflammatory disorders, including rheumatoid arthritis (RA). Activation of these cells results in the production of various mediators responsible for inflammation and RA pathogenesis. On the other hand, the depletion of macrophages using specific antibodies or chemical agents can prevent their synovial tissue infiltration and subsequently attenuates inflammation. Their plasticity is a major feature that helps the switch from a pro-inflammatory phenotype (M1) to an anti-inflammatory state (M2). Therefore, understanding the precise strategy targeting pro-inflammatory monocytes/macrophages should be a powerful way of inhibiting chronic inflammation and bone erosion. In this review, we demonstrate potential consequences of different epigenetic regulations on inflammatory cytokines production by monocytes. In addition, we present unique profiles of monocytes/macrophages contributing to identification of new biomarkers of disease activity or predicting treatment response in RA. We also outline novel approaches of tuning monocytes/macrophages by biologic drugs, small molecules or by other therapeutic modalities to reduce arthritis. Finally, the importance of cellular heterogeneity of monocytes/macrophages is highlighted by single-cell technologies, which leads to the design of cell-specific therapeutic protocols for personalized medicine in RA in the future. Full article
(This article belongs to the Special Issue Innate Immune System in Immune-Mediated Inflammatory Diseases (IMIDs))
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