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Immune Factors, Immune Cells and Inflammatory Diseases
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Immune Factors, Immune Cells and Inflammatory 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 (20 September 2023) | Viewed by 12285

Special Issue Editor

Prof. Dr. Alister C. Ward

E-Mail Website
Guest Editor
School of Medicine, Centre of Molecular and Medical Research, Deakin University, Waurn Ponds, VIC 3216, Australia
Interests: cytokines; cell signaling; JAK-STAT pathway; SOCS; hematopoiesis; leukocytes lymphocytes; leukemia; lymphoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The challenges of infection, injury, and malignancy must be constantly combatted throughout the life course in order to maintain health. This requires a sophisticated array of highly specialized immune cells, the development, and function of which are facilitated by a network of factors, including cytokines and chemokines. These immune cells act via both the innate and adaptive arms of the immune system to elicit an appropriate response. Transient inflammation represents an essential facet of this response, but chronic inflammation is associated with a range of disease states.

This Special Issue, entitled "Immune Factors, Immune Cells, and Inflammatory Diseases", seeks high-quality research articles and reviews that serve to highlight the key immune factors and cells required for normal immune cell development and function as well as their perturbation in a variety of inflammatory disease states and extending to therapies used to treat these diseases.

Prof. Dr. Alister C. Ward
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

  • cytokines
  • chemokines
  • leucocytes
  • lymphocytes
  • immunity
  • inflammation

Published Papers (7 papers)

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Editorial

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2 pages, 147 KiB  
Editorial
Immune Factors, Immune Cells and Inflammatory Diseases
by Alister C. Ward
Int. J. Mol. Sci. 2024, 25(4), 2417; https://doi.org/10.3390/ijms25042417 - 19 Feb 2024
Viewed by 580
Abstract
The immune system comprises distinct innate and adaptive arms, each of which contains many layers to provide a coordinated, sequential immune response to insults [...] Full article
(This article belongs to the Special Issue Immune Factors, Immune Cells and Inflammatory Diseases)

Research

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10 pages, 1548 KiB  
Communication
The Role of Cytokine-Inducible SH2 Domain-Containing Protein (CISH) in the Regulation of Basal and Cytokine-Mediated Myelopoiesis
by Wasan Naser, Saeed Maymand, Daniel Dlugolenski, Faiza Basheer and Alister C. Ward
Int. J. Mol. Sci. 2023, 24(16), 12757; https://doi.org/10.3390/ijms241612757 - 14 Aug 2023
Cited by 4 | Viewed by 1203
Abstract
Cytokine-inducible SH2 domain-containing protein (CISH) is a member of the suppressor of cytokine signaling (SOCS) family of negative feedback regulators shown to play crucial roles in lymphoid cell development and function as well as appetite regulation. It has also been implicated in the [...] Read more.
Cytokine-inducible SH2 domain-containing protein (CISH) is a member of the suppressor of cytokine signaling (SOCS) family of negative feedback regulators shown to play crucial roles in lymphoid cell development and function as well as appetite regulation. It has also been implicated in the control of signaling downstream of the receptors for the cytokines granulocyte/macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) in myeloid cells. To investigate the physiological role of CISH in myelopoiesis, mice deficient in CISH were analyzed basally and in response to administration of these cytokines. CISH knockout (KO) mice possessed basally elevated neutrophils in the blood, bone marrow, and spleen compared to wild-type (WT) mice. During GM-CSF-induced myelopoiesis, the frequency of neutrophils, myeloid dendritic cells (DCs), and CFU-M in the bone marrow was higher in the KO, as were the neutrophils and CFU-G in the spleen. In contrast, no differences were observed between KO and WT mice during G-CSF-induced myelopoiesis apart from an elevated frequency of CFU-G and CFU-M in the spleen. This work has identified a role for CISH in the negative regulation of granulopoiesis, including that mediated by GM-CSF. Full article
(This article belongs to the Special Issue Immune Factors, Immune Cells and Inflammatory Diseases)
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15 pages, 1697 KiB  
Article
JAK Signaling Is Critically Important in Cytokine-Induced Viral Susceptibility of Keratinocytes
by Kimberly A. Arnold, Liam F. Peterson, Lisa A. Beck and Matthew G. Brewer
Int. J. Mol. Sci. 2023, 24(11), 9243; https://doi.org/10.3390/ijms24119243 - 25 May 2023
Cited by 2 | Viewed by 1705
Abstract
Little is known about whether type 1 (IFNγ), 2 (IL-4/IL-13), or 3 (IL-17A/IL-22) cytokines affect the susceptibility of keratinocytes (KC) to viruses. These immune pathways predominate in various skin diseases: lupus, atopic dermatitis (AD), and psoriasis, respectively. Janus kinase inhibitors (JAKi) are approved [...] Read more.
Little is known about whether type 1 (IFNγ), 2 (IL-4/IL-13), or 3 (IL-17A/IL-22) cytokines affect the susceptibility of keratinocytes (KC) to viruses. These immune pathways predominate in various skin diseases: lupus, atopic dermatitis (AD), and psoriasis, respectively. Janus kinase inhibitors (JAKi) are approved to treat both AD and psoriasis, and are in clinical development for lupus. We evaluated whether these cytokines alter viral susceptibility of KC and determined if this effect is modulated by treatment with JAKi. Viral susceptibility to vaccinia virus (VV) or herpes simplex virus-1 (HSV-1) ± JAKi was assessed in immortalized and primary human KC pretreated with cytokines. Exposure to type 2 (IL-4 + IL-13) or the type 3 (IL-22) cytokines significantly increased KC viral susceptibility. Specifically, there was a peak increase of 12.2 ± 3.1-fold (IL-4 + IL-13) or 7.7 ± 2.8-fold (IL-22) in VV infection as measured by plaque number. Conversely, IFNγ significantly reduced susceptibility to VV (63.1 ± 64.4-fold). The IL-4 + IL-13-induced viral susceptibility was reduced (44 ± 16%) by JAK1 inhibition, while the IL-22-enhanced viral susceptibility was diminished (76 ± 19%) by TYK2 inhibition. IFNγ-mediated resistance to viral infection was reversed by JAK2 inhibition (366 ± 294% increase in infection). Cytokines expressed in AD skin (IL-4, IL-13, IL-22) increase KC viral susceptibility while IFNγ is protective. JAKi that target JAK1 or TYK2 reversed cytokine-enhanced viral susceptibility, while JAK2 inhibition reduced the protective effects of IFNγ. Full article
(This article belongs to the Special Issue Immune Factors, Immune Cells and Inflammatory Diseases)
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9 pages, 1813 KiB  
Communication
Effect of VEGF Stimulation on CD11b Receptor on Peripheral Eosinophils in Asthmatics
by Krzysztof Gomułka, Maciej Tota and Kacper Brzdąk
Int. J. Mol. Sci. 2023, 24(10), 8880; https://doi.org/10.3390/ijms24108880 - 17 May 2023
Cited by 2 | Viewed by 1124
Abstract
Asthma is a chronic, complex disease associated with heterogeneity in molecular pathways. Airway inflammation with different cell activation (e.g., eosinophils) and with hypersecretion of many cytokines (e.g., vascular endothelial growth factor—VEGF) might be relevant for asthma pathogenesis and responsible for airway hyperresponsiveness and [...] Read more.
Asthma is a chronic, complex disease associated with heterogeneity in molecular pathways. Airway inflammation with different cell activation (e.g., eosinophils) and with hypersecretion of many cytokines (e.g., vascular endothelial growth factor—VEGF) might be relevant for asthma pathogenesis and responsible for airway hyperresponsiveness and remodeling. The aim of our study was to reveal the expression of activation marker CD11b on peripheral eosinophils unstimulated and after VEGF in vitro stimulation in asthmatics with different degrees of airway narrowing. The study population included a total of 118 adult subjects: 78 patients with asthma (among them 39 patients with irreversible bronchoconstriction and 39 patients with reversible bronchoconstriction according to the bronchodilation test) and 40 healthy participants as a control group. CD11b expression on peripheral blood eosinophils was detected in vitro using the flow cytometric method without exogenous stimulation (negative control), after N-formyl-methionine-leucyl-phenylalanine stimulation (fMLP; positive control) and after stimulation with VEGF in two concentrations (250 ng/mL and 500 ng/mL). CD11b marker was slightly presented on unstimulated eosinophils in asthmatics and the subgroup with irreversible airway narrowing (p = 0.06 and p = 0.07, respectively). Stimulation with VEGF enhanced the activity of peripheral eosinophils and induced CD11b expression in asthmatics in comparison with a healthy control (p < 0.05), but it was dependent neither on the concentration of VEGF nor on the degree of airways narrowing in patients with asthma. We present our findings to draw attention to the potential role of VEGF in the eosinophil priming and CD11b-mediated signaling in patients with asthma which is currently undervalued. Full article
(This article belongs to the Special Issue Immune Factors, Immune Cells and Inflammatory Diseases)
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15 pages, 2729 KiB  
Article
Characterization of Ly108-H1 Signaling Reveals Ly108-3 Expression and Additional Strain-Specific Differences in Lupus Prone Mice
by Svend Rietdijk, Marton Keszei, Wilson Castro, Cox Terhorst and Ana C. Abadía-Molina
Int. J. Mol. Sci. 2023, 24(5), 5024; https://doi.org/10.3390/ijms24055024 - 6 Mar 2023
Viewed by 1475
Abstract
Ly108 (SLAMF6) is a homophilic cell surface molecule that binds SLAM-associated protein (SAP), an intracellular adapter protein that modulates humoral immune responses. Furthermore, Ly108 is crucial for the development of natural killer T (NKT) cells and CTL cytotoxicity. Significant attention has been paid [...] Read more.
Ly108 (SLAMF6) is a homophilic cell surface molecule that binds SLAM-associated protein (SAP), an intracellular adapter protein that modulates humoral immune responses. Furthermore, Ly108 is crucial for the development of natural killer T (NKT) cells and CTL cytotoxicity. Significant attention has been paid towards expression and function of Ly108 since multiple isoforms were identified, i.e., Ly108-1, Ly108-2, Ly108-3, and Ly108-H1, some of which are differentially expressed in several mouse strains. Surprisingly, Ly108-H1 appeared to protect against disease in a congenic mouse model of Lupus. Here, we use cell lines to further define Ly108-H1 function in comparison with other isoforms. We show that Ly108-H1 inhibits IL-2 production while having little effect upon cell death. With a refined method, we could detect phosphorylation of Ly108-H1 and show that SAP binding is retained. We propose that Ly108-H1 may regulate signaling at two levels by retaining the capability to bind its extracellular as well as intracellular ligands, possibly inhibiting downstream pathways. In addition, we detected Ly108-3 in primary cells and show that this isoform is also differentially expressed between mouse strains. The presence of additional binding motifs and a non-synonymous SNP in Ly108-3 further extends the diversity between murine strains. This work highlights the importance of isoform awareness, as inherent homology can present a challenge when interpreting mRNA and protein expression data, especially as alternatively splicing potentially affects function. Full article
(This article belongs to the Special Issue Immune Factors, Immune Cells and Inflammatory Diseases)
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19 pages, 6230 KiB  
Article
Identification of Key Biomarkers Associated with Immunogenic Cell Death and Their Regulatory Mechanisms in Severe Acute Pancreatitis Based on WGCNA and Machine Learning
by Zhengjian Wang, Jin Liu, Yuting Wang, Hui Guo, Fan Li, Yinan Cao, Liang Zhao and Hailong Chen
Int. J. Mol. Sci. 2023, 24(3), 3033; https://doi.org/10.3390/ijms24033033 - 3 Feb 2023
Cited by 11 | Viewed by 3634
Abstract
Immunogenic cell death (ICD) is a form of programmed cell death with a strong sense of inflammatory detection, whose powerful situational awareness can cause the reactivation of aberrant immunity. However, the role of ICD in the pathogenesis of severe acute pancreatitis (SAP) has [...] Read more.
Immunogenic cell death (ICD) is a form of programmed cell death with a strong sense of inflammatory detection, whose powerful situational awareness can cause the reactivation of aberrant immunity. However, the role of ICD in the pathogenesis of severe acute pancreatitis (SAP) has yet to be investigated. This study aims to explore the pivotal genes associated with ICD in SAP and how they relate to immune infiltration and short-chain fatty acids (SCFAs), in order to provide a theoretical foundation for further, in-depth mechanistic studies. We downloaded GSE194331 datasets from the Gene Expression Omnibus (GEO). The use of differentially expressed gene (DEG) analysis; weighted gene co-expression network analysis (WGCNA) and least absolute shrinkage and selection operator (LASSO) regression analysis allowed us to identify a total of three ICD-related hub genes (LY96, BCL2, IFNGR1) in SAP. Furthermore, single sample gene set enrichment analysis (ssGSEA) demonstrated that hub genes are closely associated with the infiltration of specific immune cells, the activation of immune pathways and the metabolism of SCFAs (especially butyrate). These findings were validated through the analysis of gene expression patterns in both clinical patients and rat animal models of SAP. In conclusion, the first concept of ICD in the pathogenesis of SAP was proposed in our study. This has important implications for future investigations into the pro-inflammatory immune mechanisms mediated by damage-associated molecular patterns (DAMPs) in the late stages of SAP. Full article
(This article belongs to the Special Issue Immune Factors, Immune Cells and Inflammatory Diseases)
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Review

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12 pages, 1048 KiB  
Review
The Role of LFA-1 for the Differentiation and Function of Regulatory T Cells—Lessons Learned from Different Transgenic Mouse Models
by Tanja Klaus, Alicia Wilson, Michael Fichter, Matthias Bros, Tobias Bopp and Stephan Grabbe
Int. J. Mol. Sci. 2023, 24(7), 6331; https://doi.org/10.3390/ijms24076331 - 28 Mar 2023
Cited by 2 | Viewed by 1632
Abstract
Regulatory T cells (Treg) are essential for the maintenance of peripheral tolerance. Treg dysfunction results in diverse inflammatory and autoimmune diseases with life-threatening consequences. β2-integrins (CD11a-d/CD18) play important roles in the migration of leukocytes into inflamed tissues and cell signaling. Of [...] Read more.
Regulatory T cells (Treg) are essential for the maintenance of peripheral tolerance. Treg dysfunction results in diverse inflammatory and autoimmune diseases with life-threatening consequences. β2-integrins (CD11a-d/CD18) play important roles in the migration of leukocytes into inflamed tissues and cell signaling. Of all β2-integrins, T cells, including Treg, only express CD11a/CD18, termed lymphocyte function-associated antigen 1 (LFA-1), on their surface. In humans, loss-of-function mutations in the common subunit CD18 result in leukocyte adhesion deficiency type-1 (LAD-1). Clinical symptoms vary depending on the extent of residual β2-integrin function, and patients may experience leukocytosis and recurrent infections. Some patients can develop autoimmune diseases, but the immune processes underlying the paradoxical situation of immune deficiency and autoimmunity have been scarcely investigated. To understand this complex phenotype, different transgenic mouse strains with a constitutive knockout of β2-integrins have been established. However, since a constitutive knockout affects all leukocytes and may limit the validity of studies focusing on their cell type-specific role, we established a Treg-specific CD18-floxed mouse strain. This mini-review aims to delineate the role of LFA-1 for the induction, maintenance, and regulatory function of Treg in vitro and in vivo as deduced from observations using the various β2-integrin-deficient mouse models. Full article
(This article belongs to the Special Issue Immune Factors, Immune Cells and Inflammatory Diseases)
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