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Cytokines in Inflammatory Signaling: 2nd Edition
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Cytokines in Inflammatory Signaling: 2nd Edition

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: 20 August 2025 | Viewed by 12600

Special Issue Editors

Dr. Waipo Chong

E-Mail Website
Guest Editor
School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China
Interests: immunology; autoimmunity; cancer
Special Issues, Collections and Topics in MDPI journals
Dr. Daniela Novick

E-Mail Website
Guest Editor
Department of Molecular Genetics, Weizmann Institute of Science Israel, Rehovot, Israel
Interests: inflammation; molecular biology; immunology; signaling pathways; biochemistry; autoimmune disease; cell biology; methods; Interleukin-18 (IL-18); IL-18 binding protein, cytokines and cytokines receptors
Special Issues, Collections and Topics in MDPI journals
Dr. Rosalinda Sorrentino

E-Mail Website
Guest Editor
Department of Pharmacy (DIFARMA), University of Salerno, Salerno, Italy
Interests: immunotherapy and target therapy; cancer; inflammation; immunity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cytokines are produced by the host immune system for the control of microbial pathogens. They are involved in cell proliferation, survival, apoptosis, differentiation, and activation. However, their dysregulation can lead to undesired pathogenic inflammation and/or autoimmune diseases, such as multiple sclerosis, uveitis, rheumatoid arthritis, inflammatory bowel disease, and systemic lupus erythematosus. This is achieved by activating various cell types, including fibroblasts, endothelial cells, epithelial cells, and immune cells, through different signalling pathways. Therefore, understanding the molecular mechanisms underlying the regulation of these cells by cytokines is important. This Special Issue aims to define the specific pathways that are influenced by cytokines during inflammation, as well as develop new therapeutics to more effectively target proinflammatory diseases.

Dr. Daniela Novick
Dr. Waipo Chong
Dr. Rosalinda Sorrentino
Guest Editors

Manuscript Submission Information

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Keywords

  • cytokines
  • inflammation
  • autoimmune diseases
  • immune homeostasis
  • signaling pathway
  • immunotherapy

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Related Special Issue

Published Papers (6 papers)

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Research

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14 pages, 4645 KiB  
Article
Chronic Low-Level IFN-γ Expression Disrupts Mitochondrial Complex I Activity in Renal Macrophages: An Early Mechanistic Driver of Lupus Nephritis Pathogenesis
by Heekyong R. Bae, Su-Kyung Shin, Ji-Yoon Lee, Yeo Jin Ko, Suntae Kim, Howard A. Young and Eun-Young Kwon
Int. J. Mol. Sci. 2025, 26(1), 63; https://doi.org/10.3390/ijms26010063 - 25 Dec 2024
Viewed by 903
Abstract
Mitochondrial dysfunction and macrophage dysregulation are well recognized as significant contributors to the pathogenesis of autoimmune diseases. However, the detailed mechanisms connecting these two factors remain poorly understood. This study hypothesizes that low but chronic interferon-gamma (IFN-γ) plays a critical role in these [...] Read more.
Mitochondrial dysfunction and macrophage dysregulation are well recognized as significant contributors to the pathogenesis of autoimmune diseases. However, the detailed mechanisms connecting these two factors remain poorly understood. This study hypothesizes that low but chronic interferon-gamma (IFN-γ) plays a critical role in these processes. To explore this, we utilized ARE-Del mice, a model characterized by sustained low-level IFN-γ expression and lupus nephritis (LN)-like symptoms. Age- and tissue-dependent gene expression analyses in ARE-Del mice revealed significant suppression of mitochondrial complex I components and activities, particularly in the kidneys. The genotype-dependent suppression of mitochondrial complex I indicates early disruption, which leads to macrophage dysfunction. Notably, remission restored gene expression of mitochondrial complex I and macrophage dysfunction in isolated renal macrophages from NZB/W lupus-prone mice. These findings suggest that chronic low-level IFN-γ disrupts mitochondrial complex I activity in macrophages, highlighting its role in the early pathogenesis of autoimmune diseases like lupus nephritis. This provides new insights into the molecular interactions underlying autoimmune pathogenesis and suggests potential targets for therapeutic intervention. Full article
(This article belongs to the Special Issue Cytokines in Inflammatory Signaling: 2nd Edition)
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17 pages, 298 KiB  
Article
Could Selected Adipokines/Cytokines Serve as Markers of Adipose Tissue Dysfunction?
by Lucyna Ostrowska, Joanna Smarkusz-Zarzecka, Beata Zyśk, Karolina Orywal, Barbara Mroczko and Urszula Cwalina
Int. J. Mol. Sci. 2024, 25(24), 13744; https://doi.org/10.3390/ijms252413744 - 23 Dec 2024
Viewed by 756
Abstract
Elevated levels of pro-inflammatory adipokines and cytokines increase the risk of developing metabolic disorders and diseases. The aim of this study was to conduct a comparative analysis of selected adipokines/cytokines in the blood serum of adults with obesity and normal body weight. The [...] Read more.
Elevated levels of pro-inflammatory adipokines and cytokines increase the risk of developing metabolic disorders and diseases. The aim of this study was to conduct a comparative analysis of selected adipokines/cytokines in the blood serum of adults with obesity and normal body weight. The study also evaluated the correlation of these adipokines/cytokines with selected biochemical blood parameters. The study included 46 individuals with first- and second-degree obesity and 35 individuals with normal body weight. The participants underwent nutritional status assessments, biochemical tests, and evaluations of adipokine and cytokine concentrations in blood serum. The study found higher median CRP concentrations in women with obesity than in those with normal weight. This increase was statistically significant. The results also showed significantly higher IL-6 levels in the obesity group compared to the control group in both women and men. Resistin and MMP-2 were significantly different between women with obesity and women with normal body weight. Multiple regression results indicated that higher total fat content was significantly associated with higher serum CRP and IL-6 levels and lower adiponectin levels. Interleukin 6 was the strongest predictor of adipose tissue dysfunction in both women and men. Potential markers in women could also include resistin and MMP-2. The findings suggest that gender significantly influences the regulation of inflammatory factors. Full article
(This article belongs to the Special Issue Cytokines in Inflammatory Signaling: 2nd Edition)
16 pages, 3206 KiB  
Article
Differential Fatty Acid Response of Resident Macrophages in Human Skeletal Muscle Fiber and Intermuscular Adipose Tissue
by Xiaoying Chen, Aline Müller, Miguel Pishnamaz, Frank Hildebrand, Leo Cornelius Bollheimer and Mahtab Nourbakhsh
Int. J. Mol. Sci. 2024, 25(19), 10722; https://doi.org/10.3390/ijms251910722 - 5 Oct 2024
Cited by 2 | Viewed by 1227
Abstract
Human skeletal muscle contains different types of tissues with skeletal muscle fibers (SMFs) and intermuscular adipose tissues (IMATs) as the main components. We maintained human skeletal muscle tissues from 12 study participants under native conditions in vitro for 11 days to investigate the [...] Read more.
Human skeletal muscle contains different types of tissues with skeletal muscle fibers (SMFs) and intermuscular adipose tissues (IMATs) as the main components. We maintained human skeletal muscle tissues from 12 study participants under native conditions in vitro for 11 days to investigate the dynamics of macrophages that reside in adjacent IMATs and SMFs simultaneously. The samples were subjected to immunohistochemical analysis for macrophage phenotyping and mitochondrial mass assessment before and after maintenance in vitro. Multiplex protein analysis was used to determine cytokine/chemokine expression in tissue extracts. The results revealed significant correlations between donor age or body mass index (BMI) and distinct phenotypes of resident macrophages in SMFs and IMATs. The dynamics of SMF- and IMAT-resident macrophages differed significantly in vitro and exhibited inverse correlations with chemokine/cytokine expression levels and mitochondrial activity. Moreover, the responses of macrophages to saturated and unsaturated fatty acids (FAs) differed substantially between SMFs and IMATs. These findings showed the functional diversity of phenotypically identical macrophages in adjacent niches. Thus, the currently available macrophage markers cannot capture the functional diversity of human tissue-resident macrophages. The model used in the present study may help elucidate how macrophages affect muscle homeostasis and disease in humans. Full article
(This article belongs to the Special Issue Cytokines in Inflammatory Signaling: 2nd Edition)
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18 pages, 3289 KiB  
Article
Reduction in Hippocampal Amyloid-β Peptide (Aβ) Content during Glycine-Proline-Glutamate (Gly-Pro-Glu) Co-Administration Is Associated with Changes in Inflammation and Insulin-like Growth Factor (IGF)-I Signaling
by Laura M. Frago, Emma Burgos-Ramos, María Rodríguez-Pérez, Sandra Canelles, Eduardo Arilla-Ferreiro, Jesús Argente, Manuela G. López and Vicente Barrios
Int. J. Mol. Sci. 2024, 25(11), 5716; https://doi.org/10.3390/ijms25115716 - 24 May 2024
Cited by 1 | Viewed by 1432
Abstract
Alzheimer’s disease (AD) is characterized by the deposition in the brain of senile plaques composed of amyloid-β peptides (Aβs) that increase inflammation. An endogenous peptide derived from the insulin-like growth factor (IGF)-I, glycine-proline-glutamate (GPE), has IGF-I-sensitizing and neuroprotective actions. Here, we examined the [...] Read more.
Alzheimer’s disease (AD) is characterized by the deposition in the brain of senile plaques composed of amyloid-β peptides (Aβs) that increase inflammation. An endogenous peptide derived from the insulin-like growth factor (IGF)-I, glycine-proline-glutamate (GPE), has IGF-I-sensitizing and neuroprotective actions. Here, we examined the effects of GPE on Aβ levels and hippocampal inflammation generated by the intracerebroventricular infusion of Aβ25-35 for 2 weeks (300 pmol/day) in ovariectomized rats and the signaling-related pathways and levels of Aβ-degrading enzymes associated with these GPE-related effects. GPE prevented the Aβ-induced increase in the phosphorylation of p38 mitogen-activated protein kinase and the reduction in activation of signal transducer and activator of transcription 3, insulin receptor substrate-1, and Akt, as well as on interleukin (IL)-2 and IL-13 levels in the hippocampus. The functionality of somatostatin, measured as the percentage of inhibition of adenylate cyclase activity and the levels of insulin-degrading enzyme, was also preserved by GPE co-treatment. These findings indicate that GPE co-administration may protect from Aβ insult by changing hippocampal cytokine content and somatostatin functionality through regulation of leptin- and IGF-I-signaling pathways that could influence the reduction in Aβ levels through modulation of levels and/or activity of Aβ proteases. Full article
(This article belongs to the Special Issue Cytokines in Inflammatory Signaling: 2nd Edition)
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Review

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24 pages, 3292 KiB  
Review
Unraveling Macrophage Polarization: Functions, Mechanisms, and “Double-Edged Sword” Roles in Host Antiviral Immune Responses
by Meng Yao, Meilin Li, Dingkun Peng, Yijing Wang, Su Li, Ding Zhang, Bo Yang, Hua-Ji Qiu and Lian-Feng Li
Int. J. Mol. Sci. 2024, 25(22), 12078; https://doi.org/10.3390/ijms252212078 - 10 Nov 2024
Cited by 1 | Viewed by 2198
Abstract
Numerous viruses that propagate through the respiratory tract may be initially engulfed by macrophages (Mφs) within the alveoli, where they complete their first replication cycle and subsequently infect the adjacent epithelial cells. This process can lead to significant pathological damage to [...] Read more.
Numerous viruses that propagate through the respiratory tract may be initially engulfed by macrophages (Mφs) within the alveoli, where they complete their first replication cycle and subsequently infect the adjacent epithelial cells. This process can lead to significant pathological damage to tissues and organs, leading to various diseases. As essential components in host antiviral immune systems, Mφs can be polarized into pro-inflammatory M1 Mφs or anti-inflammatory M2 Mφs, a process involving multiple signaling pathways and molecular mechanisms that yield diverse phenotypic and functional features in response to various stimuli. In general, when infected by a virus, M1 macrophages secrete pro-inflammatory cytokines to play an antiviral role, while M2 macrophages play an anti-inflammatory role to promote the replication of the virus. However, recent studies have shown that some viruses may exhibit the opposite trend. Viruses have evolved various strategies to disrupt Mφ polarization for efficient replication and transmission. Notably, various factors, such as mechanical softness, the altered pH value of the endolysosomal system, and the homeostasis between M1/M2 Mφs populations, contribute to crucial events in the viral replication cycle. Here, we summarize the regulation of Mφ polarization, virus-induced alterations in Mφ polarization, and the antiviral mechanisms associated with these changes. Collectively, this review provides insights into recent advances regarding Mφ polarization in host antiviral immune responses, which will contribute to the development of precise prevention strategies as well as management approaches to disease incidence and transmission. Full article
(This article belongs to the Special Issue Cytokines in Inflammatory Signaling: 2nd Edition)
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15 pages, 1509 KiB  
Review
Roles of Cytokines in Alzheimer’s Disease
by Zilin Chen, Yekkuni L. Balachandran, Wai Po Chong and Kannie W. Y. Chan
Int. J. Mol. Sci. 2024, 25(11), 5803; https://doi.org/10.3390/ijms25115803 - 26 May 2024
Cited by 13 | Viewed by 4743
Abstract
The neuroimmune system is a collection of immune cells, cytokines, and the glymphatic system that plays a pivotal role in the pathogenesis and progression of Alzheimer’s disease (AD). Of particular focus are cytokines, a group of immune signaling molecules that facilitate communication among [...] Read more.
The neuroimmune system is a collection of immune cells, cytokines, and the glymphatic system that plays a pivotal role in the pathogenesis and progression of Alzheimer’s disease (AD). Of particular focus are cytokines, a group of immune signaling molecules that facilitate communication among immune cells and contribute to inflammation in AD. Extensive research has shown that the dysregulated secretion of certain cytokines (IL-1β, IL-17, IL-12, IL-23, IL-6, and TNF-α) promotes neuroinflammation and exacerbates neuronal damage in AD. However, anti-inflammatory cytokines (IL-2, IL-3, IL-33, and IL-35) are also secreted during AD onset and progression, thereby preventing neuroinflammation. This review summarizes the involvement of pro- and anti-inflammatory cytokines in AD pathology and discusses their therapeutic potential. Full article
(This article belongs to the Special Issue Cytokines in Inflammatory Signaling: 2nd Edition)
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