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Cytokines in Immune Diseases
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Cytokines in Immune Diseases

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 (30 September 2024) | Viewed by 8113

Special Issue Editor

Prof. Dr. Pio Conti

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Guest Editor
Postgraduate Medical School, University of Chieti, Chieti, Italy
Interests: inflammation; innate immunity; cell culture; immunology of infectious diseases; psoriasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Immune cells are ubiquitously distributed in our organism, and are sources of biologically active compounds such as cytokines/chemokines and growth factors. They also mediate innate and adaptive immunity. The increased concentration of cytokines in humans causes local and systemic inflammation, which can even lead to death. Chemokines, interleukins, lymphokines, interferons, and tumour necrosis factors are common cytokines related to immune responses. As we know, cytokines play an important role in immune diseases, such as immunological disorders, tumour immunology, asthma, allergies, etc. These topics are very intricate and deserve thorough investigation.

In this Special Issue, original research articles and comprehensive reviews on the topic of cytokines in immune diseases are warmly welcomed by outstanding experts in the research area.

Prof. Dr. Pio Conti
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.

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Published Papers (4 papers)

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Research

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13 pages, 6156 KiB  
Article
Nerve Growth Factor Signaling Modulates the Expression of Glutaminase in Dorsal Root Ganglion Neurons during Peripheral Inflammation
by Vikramsingh Gujar, Radhika D. Pande, Bhalchandra M. Hardas and Subhas Das
Int. J. Mol. Sci. 2024, 25(11), 6053; https://doi.org/10.3390/ijms25116053 - 31 May 2024
Cited by 1 | Viewed by 990
Abstract
Glutamate functions as the major excitatory neurotransmitter for primary sensory neurons and has a crucial role in sensitizing peripheral nociceptor terminals producing sensitization. Glutaminase (GLS) is the synthetic enzyme that converts glutamine to glutamate. GLS-immunoreactivity (-ir) and enzyme activity are elevated in dorsal [...] Read more.
Glutamate functions as the major excitatory neurotransmitter for primary sensory neurons and has a crucial role in sensitizing peripheral nociceptor terminals producing sensitization. Glutaminase (GLS) is the synthetic enzyme that converts glutamine to glutamate. GLS-immunoreactivity (-ir) and enzyme activity are elevated in dorsal root ganglion (DRG) neuronal cell bodies during chronic peripheral inflammation, but the mechanism for this GLS elevation is yet to be fully characterized. It has been well established that, after nerve growth factor (NGF) binds to its high-affinity receptor tropomyosin receptor kinase A (TrkA), a retrograde signaling endosome is formed. This endosome contains the late endosomal marker Rab7GTPase and is retrogradely transported via axons to the cell soma located in the DRG. This complex is responsible for regulating the transcription of several critical nociceptive genes. Here, we show that this retrograde NGF signaling mediates the expression of GLS in DRG neurons during the process of peripheral inflammation. We disrupted the normal NGF/TrkA signaling in adjuvant-induced arthritic (AIA) Sprague Dawley rats by the pharmacological inhibition of TrkA or blockade of Rab7GTPase, which significantly attenuated the expression of GLS in DRG cell bodies. The results indicate that NGF/TrkA signaling is crucial for the production of glutamate and has a vital role in the development of neurogenic inflammation. In addition, our pain behavioral data suggest that Rab7GTPase can be a potential target for attenuating peripheral inflammatory pain. Full article
(This article belongs to the Special Issue Cytokines in Immune Diseases)
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14 pages, 3406 KiB  
Article
The Interaction of HMGB1 with the Proinflammatory TREM-1 Receptor Generates Cytotoxic Lymphocytes Active against HLA-Negative Tumor Cells
by Daria M. Yurkina, Elena A. Romanova, Alexey V. Feoktistov, Natalia V. Soshnikova, Anna V. Tvorogova, Denis V. Yashin and Lidia P. Sashchenko
Int. J. Mol. Sci. 2024, 25(1), 627; https://doi.org/10.3390/ijms25010627 - 3 Jan 2024
Viewed by 1673
Abstract
High mobility group protein (HMGB1) is secreted by myeloid cells and cells of damaged tissues during inflammation, causing inflammatory reactions through various receptors, including TLRS and RAGE. TREM-1 is considered to be one of the potential HMGB1 receptors. In this work, we [...] Read more.
High mobility group protein (HMGB1) is secreted by myeloid cells and cells of damaged tissues during inflammation, causing inflammatory reactions through various receptors, including TLRS and RAGE. TREM-1 is considered to be one of the potential HMGB1 receptors. In this work, we have shown that the HMGB1 protein is able to bind to the TREM-1 receptor at high affinity both in solution and on the cell surface. This binding causes lymphocytes to release cytokines IL-2, IL-1b, IL-6, TNF and Ifny into the medium, which leads to the appearance of cytotoxic lymphocytes in PBMC capable of lysing HLA-negative tumor cells. Expanding the spectra of proinflammatory receptor ligands and understanding the mechanisms of their action is essential for the creation of new immunotherapy pathways. Full article
(This article belongs to the Special Issue Cytokines in Immune Diseases)
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Review

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16 pages, 1766 KiB  
Review
Impact of TNF and IL-33 Cytokines on Mast Cells in Neuroinflammation
by Pio Conti, Gianpaolo Ronconi, Dorina Lauritano, Filiberto Mastrangelo, Alessandro Caraffa, Carla E. Gallenga, Ilias Frydas, Spyridon K. Kritas, Francesco Carinci, Federico Gaudelli, Ciro Annicchiarico and Cristian D’Ovidio
Int. J. Mol. Sci. 2024, 25(6), 3248; https://doi.org/10.3390/ijms25063248 - 13 Mar 2024
Cited by 3 | Viewed by 2362
Abstract
Mast cells (MCs) are derived from hematopoietic progenitors, mature in vascularized tissues, and participate in innate and acquired immunity. Neuroinflammation is a highly debated topic in the biomedical literature; however, the impact of tumor necrosis factor (TNF) and IL-33 on MCs in the [...] Read more.
Mast cells (MCs) are derived from hematopoietic progenitors, mature in vascularized tissues, and participate in innate and acquired immunity. Neuroinflammation is a highly debated topic in the biomedical literature; however, the impact of tumor necrosis factor (TNF) and IL-33 on MCs in the brain has not been widely addressed. MCs can be activated by IgE binding to FcεRI, as well as by different antigens. After activation, MCs mediate various immunological and inflammatory responses through TNF and IL-33. TNF has two receptors: TNFR1, a p55 molecule, and TNFR2, a p75 molecule. This cytokine is the only one of its kind to be stored in the granules of MCs and can also be generated by de novo synthesis via mRNA. In the central nervous system (CNS), TNF is produced almost exclusively by microglial cells, neurons, astrocytes, and, minimally, by endothelial cells. After its release into brain tissue, TNF rapidly induces the adhesion molecules endothelial leukocyte adhesion molecule 1 (ELAM-1), intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) in endothelial cells. TNF causes the chemoattraction of neutrophils by inducing several molecules, including CXC chemokines (IL-8). Both MCs and microglial cells act as a primary barrier against foreign molecules in the CNS, producing pro-inflammatory cytokines such as IL-33. IL-33 belongs to the IL-1 family, is activated through the ST2L/IL1-RAcP receptor complex, and mediates both the innate and adaptive immune response. IL-33 is a nuclear transcription factor expressed in the brain, where it induces pro-inflammatory cytokines (TNF and IL-1) and chemokines (CCL2, CCL3, CCL5, and CXCL10). Therefore, MCs and microglia in the CNS are a source of pro-inflammatory cytokines, including TNF and IL-33, that mediate many brain diseases. The inhibition of TNF and IL-33 may represent a new therapeutic approach that could complement existing neuroinflammatory therapies. Full article
(This article belongs to the Special Issue Cytokines in Immune Diseases)
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19 pages, 1630 KiB  
Review
The Role of Atypical Chemokine Receptors in Neuroinflammation and Neurodegenerative Disorders
by Hunter G. Lindsay, Colby J. Hendrix, Josue D. Gonzalez Murcia, Christopher Haynie and K. Scott Weber
Int. J. Mol. Sci. 2023, 24(22), 16493; https://doi.org/10.3390/ijms242216493 - 18 Nov 2023
Cited by 2 | Viewed by 2487
Abstract
Neuroinflammation is associated with several neurodegenerative disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). Neuroinflammation provides protection in acute situations but results in significant damage to the nervous system if chronic. Overexpression of chemokines within the brain results in [...] Read more.
Neuroinflammation is associated with several neurodegenerative disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). Neuroinflammation provides protection in acute situations but results in significant damage to the nervous system if chronic. Overexpression of chemokines within the brain results in the recruitment and activation of glial and peripheral immune cells which can propagate a cascading inflammatory response, resulting in neurodegeneration and the onset of neurodegenerative disorders. Recent work has identified the role of atypical chemokine receptors (ACKRs) in neurodegenerative conditions. ACKRs are seven-transmembrane domain receptors that do not follow canonical G protein signaling, but regulate inflammatory responses by modulating chemokine abundance, location, and availability. This review summarizes what is known about the four ACKRs and three putative ACKRs within the brain, highlighting their known expression and discussing the current understanding of each ACKR in the context of neurodegeneration. The ability of ACKRs to alter levels of chemokines makes them an appealing therapeutic target for neurodegenerative conditions. However, further work is necessary to understand the expression of several ACKRs within the neuroimmune system and the effectiveness of targeted drug therapies in the prevention and treatment of neurodegenerative conditions. Full article
(This article belongs to the Special Issue Cytokines in Immune Diseases)
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