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Antioxidants
Special Issues
Redox Regulation of Immune and Inflammatory Responses
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Redox Regulation of Immune and Inflammatory Responses

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 10 September 2026 | Viewed by 10535

Special Issue Editor

Dr. Yasuhiro Yoshida

E-Mail Website
Guest Editor
Department of Immunology and Parasitology, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan
Interests: IL-1 signaling; NF-κB; particulate matter; neutrophil
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleague,

The immune system and inflammatory responses are indispensable processes at the forefront of host defense. Recent research has illuminated the central role of strict redox (oxidation–reduction) state control within these complex biological reactions. Once considered merely cytotoxic agents, reactive oxygen species (ROS) and reactive nitrogen species (RNS) are now recognized as crucial intracellular signaling molecules, fine-tuning immune cell activation, differentiation, and the production of inflammatory cytokines. Crucially, these redox signals often converge on key transcription factors like NF-κB (Nuclear Factor kappa light chain enhancer of activated B cells), directly influencing gene expression, which is critical for inflammatory and immune responses.

This Special Issue, "Redox Regulation of Immune and Inflammatory Responses", aims to explore how the balance between oxidative stress and antioxidant defense optimizes hosts’ protective mechanisms or, conversely, contributes to pathological conditions. We focus on the functions of key antioxidant pathways like NADPH oxidase (NOX) and mitochondrial ROS production in immune cells, and the glutathione and thioredoxin systems. Particular attention will be given to how their dysregulation, often mediated through altered NF-κB activation, is implicated in the onset and progression of a wide range of diseases, including autoimmune disorders, chronic inflammation, and infections.

Deepening our understanding in this field will not only lead to the development of novel therapeutic strategies for inflammatory diseases, but also re-emphasize the importance of redox balance in maintaining overall health. We hope that this Special Issue serves as a bridge between redox biology and immunology, contributing to future advancements in research.

Prof. Dr. Yasuhiro Yoshida
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 250 words) can be sent to the Editorial Office for assessment.

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. Antioxidants is an international peer-reviewed open access monthly 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 2900 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

  • immune system
  • inflammatory responses
  • cytokines
  • immune cells
  • autoimmune disorders
  • chronic inflammation
  • and infections

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Published Papers (6 papers)

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Research

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13 pages, 1043 KB  
Article
Involvement of Oxidative Stress-Related Inflammatory Mediators in the Pathogenesis and Treatment Response of Macular Edema Secondary to Branch Retinal Vein Occlusion
by Takuto Yamamoto, Hidetaka Noma, Tatsuya Mimura, Shotaro Sasaki, Taro Otawa, Kanako Yasuda and Masahiko Shimura
Antioxidants 2026, 15(5), 607; https://doi.org/10.3390/antiox15050607 - 11 May 2026
Viewed by 247
Abstract
Background: Branch retinal vein occlusion (BRVO) represents a segmental retinal ischemic disorder characterized by localized oxidative–inflammatory activation. While redox-driven cytokine responses have been described in central retinal vein occlusion, their role in BRVO-specific macular edema and treatment responsiveness remains unclear. This study [...] Read more.
Background: Branch retinal vein occlusion (BRVO) represents a segmental retinal ischemic disorder characterized by localized oxidative–inflammatory activation. While redox-driven cytokine responses have been described in central retinal vein occlusion, their role in BRVO-specific macular edema and treatment responsiveness remains unclear. This study investigated whether novel redox-related inflammatory mediators in the aqueous humor are associated with disease severity and structural response to anti-vascular endothelial growth factor (VEGF) therapy in BRVO. Methods: Aqueous humor samples were collected from 30 treatment-naïve patients with BRVO and 19 control patients. Levels of VEGF and the novel redox-related inflammatory factors FMS-related tyrosine kinase 3 ligand (Flt-3L), fractalkine, CXCL-16, and endocan-1 were measured by suspension array, and the severity of macular edema was evaluated by measuring central macular thickness and neurosensory retinal thickness (TNeuro) by spectral-domain optical coherence tomography. Therapeutic response was assessed one month after intravitreal ranibizumab injection (IRI). Results: Aqueous levels of VEGF, Flt-3L, and endocan-1 were significantly higher in the BRVO group, and levels of Flt-3L, CXCL-16, and endocan-1—markers associated with oxidative endothelial damage and leukocyte recruitment—correlated significantly with each other and with aqueous flare values. Notably, baseline Flt-3L levels significantly correlated with the reduction in TNeuro, suggesting that this redox-sensitive signaling molecule is a potential biomarker for treatment sensitivity. Conclusions: These findings suggest that novel inflammatory factors, potentially driven by oxidative-nitrosative stress, play a pivotal role in the pathophysiology of BRVO. Baseline Flt-3L may serve as a predictive biomarker for structural responsiveness to anti-VEGF therapy in BRVO, suggesting that oxidative–inflammatory signaling contributes not only to disease severity but also to therapeutic heterogeneity. Full article
(This article belongs to the Special Issue Redox Regulation of Immune and Inflammatory Responses)
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17 pages, 1287 KB  
Article
Investigating the Antioxidant and Immunomodulatory Effects of Quercetin Using Porcine PBMCs as an Inflammatory In Vitro Model
by Fanni Somogyi, Nikolett Palkovicsné Pézsa, Ákos Jerzsele, Jázmin Németh, Levente Harmat and Orsolya Farkas
Antioxidants 2026, 15(3), 358; https://doi.org/10.3390/antiox15030358 - 12 Mar 2026
Viewed by 626
Abstract
As the human population continues to grow, the demand for pork increases, and the management of infectious diseases in swine from a One Health standpoint is becoming more important than ever. To prevent antimicrobial use as much as possible, the search continues for [...] Read more.
As the human population continues to grow, the demand for pork increases, and the management of infectious diseases in swine from a One Health standpoint is becoming more important than ever. To prevent antimicrobial use as much as possible, the search continues for alternative substances that can aid in mitigating oxidative stress and inflammation, which are cornerstones of infectious disease. In this study, we stimulated porcine peripheral mononuclear blood cells (pPBMCs) with either bacterial lipopolysaccharides (LPS) of different origin (Salmonella Typhimurium, Salmonella Enteritidis and E. coli), or the plant lectins concanavalin A (ConA) and phytohemagglutinin (PHA) to create an in vitro inflammatory model. Quercetin, a flavonoid with well documented positive effects, was used with the aim of decreasing oxidative stress and the production of the inflammatory cytokines IL-6 and IL-8. Oxidative stress was successfully induced in the pPBMCs by all stimulants (except for S. Enteritidis LPS), along with IL-6 production (except for E. coli LPS); IL-8 production was only induced by treatment with LPS. While quercetin had an antioxidant effect on the pPBMCs, it did not reduce IL-6 or IL-8 levels under the conditions tested and even had a pro-inflammatory effect by increasing IL-8 production when combined with LPS. To gain a deeper understanding of the immunomodulatory effects of quercetin on pPBMCs, further studies should be conducted to measure the production of additional pro- and anti-inflammatory cytokines, including TNF-α, IL-10, and IL-1β. Full article
(This article belongs to the Special Issue Redox Regulation of Immune and Inflammatory Responses)
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24 pages, 11114 KB  
Article
Deinoxanthin-Enriched Extracellular Vesicles from Deinococcus radiodurans Drive IL-10–Dependent Tolerogenic Programming of Dendritic Cells
by Jeong Moo Han, Jaeyoon Lim, Woo Sik Kim, Bo-Gyeong Yoo, Jong-Hyun Jung, Sangyong Lim and Eui-Baek Byun
Antioxidants 2025, 14(9), 1108; https://doi.org/10.3390/antiox14091108 - 12 Sep 2025
Cited by 1 | Viewed by 1773
Abstract
Extracellular vesicles (EVs) derived from bacteria are emerging as potent bioactive carriers that affect host immunity. Deinococcus radiodurans, an extremophilic bacterium with strong antioxidant capacity, produces EVs enriched in deinoxanthin (DX), a carotenoid with a reactive oxygen species–scavenging activity. Here, we assessed [...] Read more.
Extracellular vesicles (EVs) derived from bacteria are emerging as potent bioactive carriers that affect host immunity. Deinococcus radiodurans, an extremophilic bacterium with strong antioxidant capacity, produces EVs enriched in deinoxanthin (DX), a carotenoid with a reactive oxygen species–scavenging activity. Here, we assessed the antioxidant activity of D. radiodurans-derived EVs (R1-EVs) in biochemical assays and their immunomodulatory effects on dendritic cells (DCs). R1-EVs exhibited significantly higher antioxidant activity than EVs from a DX-deficient mutant strain (ΔcrtI-EVs), consistent with DX enrichment. Bone marrow-derived DCs treated with R1-EVs in the presence of lipopolysaccharide displayed reduced expression of surface maturation markers and pro-inflammatory cytokines, while interleukin-10 (IL-10) production and antigen uptake were preserved, indicating a tolerogenic phenotype. This tolerogenic program led to decreased proliferation and cytokine production in allogeneic CD4+ and CD8+ T cells. Mechanistically, R1-EVs inhibited mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling pathways, key regulators of the DC activation. Importantly, IL-10 neutralization reversed these effects, restoring DC and T cell activation. Notably, ΔcrtI-EVs showed weaker antioxidant and immunoregulatory activities. Together, our findings identify R1-EVs as dual-functions, DX- and IL-10-dependent nanoplatform that integrates antioxidant and tolerogenic properties, with potential applications in inflammatory and autoimmune disease control. Full article
(This article belongs to the Special Issue Redox Regulation of Immune and Inflammatory Responses)
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Review

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38 pages, 3027 KB  
Review
Extracellular Redox Balance as a Determinant of Immune Regulation and Tissue Inflammation
by Rebecca Seitz, Martina Müller and Karsten Gülow
Antioxidants 2026, 15(3), 280; https://doi.org/10.3390/antiox15030280 - 24 Feb 2026
Cited by 1 | Viewed by 1275
Abstract
Reactive oxygen species (ROS) are widely recognized as intracellular signaling mediators and contributors to oxidative damage. Increasing evidence indicates that redox processes in the extracellular space constitute a distinct and functionally relevant layer of immune regulation. Extracellular ROS are generated in a spatially [...] Read more.
Reactive oxygen species (ROS) are widely recognized as intracellular signaling mediators and contributors to oxidative damage. Increasing evidence indicates that redox processes in the extracellular space constitute a distinct and functionally relevant layer of immune regulation. Extracellular ROS are generated in a spatially and temporally controlled manner by immune and non-immune cells and are shaped by local antioxidant buffering, redox-active metabolites, and tissue architecture. Rather than acting as diffuse by-products of inflammation, extracellular redox conditions modulate immune cell activation, migration, and intercellular communication by influencing surface-associated signaling events and receptor responsiveness. Physiological redox control in the extracellular compartment supports host defense, tissue repair, and coordinated immune responses. In contrast, disruption of spatial redox regulation promotes chronic inflammation, immune dysfunction, cancer-associated immune suppression, and systemic inflammatory states such as sepsis. Loss of redox confinement and insufficient extracellular buffering uncouple redox signaling from its regulatory function and contribute to endothelial dysfunction, immune dysregulation, and tissue injury. Together, these observations identify the extracellular redox balance as an integral component of immune regulation with important implications for understanding inflammatory pathology and for the development of strategies that preserve localized redox control rather than globally suppressing ROS. Full article
(This article belongs to the Special Issue Redox Regulation of Immune and Inflammatory Responses)
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24 pages, 1465 KB  
Review
Melatonin at the Crossroads of Oxidative Stress, Immunity, and Cancer Therapy
by Elena Lavado-Fernández, Cristina Pérez-Montes, Miguel Robles-García, Adrián Santos-Ledo and Marina García-Macia
Antioxidants 2026, 15(1), 64; https://doi.org/10.3390/antiox15010064 - 3 Jan 2026
Cited by 4 | Viewed by 2315
Abstract
Melatonin, an ancient and evolutionarily conserved indolamine, has long attracted attention for its multifunctional roles in redox homeostasis. More recently, it has been studied in relation to immune regulation and cancer biology. Beyond its well-known circadian function, melatonin modulates oxidative stress by directly [...] Read more.
Melatonin, an ancient and evolutionarily conserved indolamine, has long attracted attention for its multifunctional roles in redox homeostasis. More recently, it has been studied in relation to immune regulation and cancer biology. Beyond its well-known circadian function, melatonin modulates oxidative stress by directly scavenging reactive oxygen and nitrogen species and by upregulating antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase. At the same time, it exerts wide-ranging immunomodulatory functions by influencing both innate and adaptive immune responses. All these actions converge within the tumor microenvironment, where oxidative stress and immune suppression drive cancer progression. Although the antitumoral effects of melatonin have traditionally been interpreted through its actions on T cells and NK cells, recent studies identify macrophages as an underappreciated and pivotal target. Notably, melatonin influences macrophage polarization, favoring antitumor M1 phenotypes over pro-tumoral M2 states, while attenuating chronic inflammation and restoring mitochondrial function. This review summarizes current knowledge on melatonin’s antioxidant and immunoregulatory mechanisms, highlighting its impact on the tumor immune microenvironment, with a particular focus on the growing recognition of macrophages as a compelling new axis through which melatonin may exert anticancer effects. Full article
(This article belongs to the Special Issue Redox Regulation of Immune and Inflammatory Responses)
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26 pages, 1051 KB  
Review
High-Altitude Hypoxia Injury: Systemic Mechanisms and Intervention Strategies on Immune and Inflammatory Responses
by Jingman Zhang, Shujie Guo, Beiebei Dou, Yang Liu, Xiaonan Wang, Yingze Jiao, Qianwen Li, Yan Li and Han Chen
Antioxidants 2026, 15(1), 36; https://doi.org/10.3390/antiox15010036 - 26 Dec 2025
Cited by 2 | Viewed by 3480
Abstract
High-altitude exposure poses significant health challenges to mountaineers, military personnel, travelers, and indigenous residents. Altitude-related illnesses encompass acute conditions such as acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE), and high-altitude cerebral edema (HACE), and chronic manifestations like chronic mountain sickness (CMS). Hypobaric [...] Read more.
High-altitude exposure poses significant health challenges to mountaineers, military personnel, travelers, and indigenous residents. Altitude-related illnesses encompass acute conditions such as acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE), and high-altitude cerebral edema (HACE), and chronic manifestations like chronic mountain sickness (CMS). Hypobaric hypoxia induces oxidative stress and inflammatory cascades, causing alterations in multiple organ systems through co-related amplification mechanisms. Therefore, this review aims to systematically discuss the injury mechanisms and comprehensive intervention strategies involved in high-altitude diseases. In summary, these pathologies involve key damage pathways: oxidative stress activates inflammatory pathways through NF-κB and NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasomes; energy depletion impairs calcium homeostasis, leading to cellular calcium overload; mitochondrial dysfunction amplifies injury through mitochondrial permeability transition pore (mPTP) opening and apoptotic factor release. These mechanisms could be converged in organ-specific patterns—blood–brain barrier disruption in HACE, stress failure in HAPE, and right heart dysfunction in chronic exposure. Promising strategies include multi-level therapeutic approaches targeting oxygenation (supplemental oxygen, acetazolamide), specific pathway modulation (antioxidants, calcium channel blockers, HIF-1α regulators), and damage repair (glucocorticoids). Notably, functional foods show significant therapeutic potential: dietary nitrates (beetroot) enhance oxygen delivery, tea polyphenols and anthocyanins (black goji berry) provide antioxidant effects, and traditional herbal bioactives (astragaloside, ginsenosides) offer multi-targeted organ protection. Full article
(This article belongs to the Special Issue Redox Regulation of Immune and Inflammatory Responses)
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