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Allergic Diseases: Molecular Pathways and Pathogenesis
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Allergic Diseases: Molecular Pathways and Pathogenesis

A Special Issue of Current Issues in Molecular Biology (ISSN 1467-3045) belonging to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 792

Editor

Dr. Jing Gao

E-Mail Website
Guest Editor
Respiratory Medicine Unit, Department of Medicine & Centre for Molecular Medicine, Karolinska Institute, 171 77 Stockholm, Sweden
Interests: respiratory diseases; infectious diseases; bioinformatics; molecular medicine; global health; landscape patterns; ecological resilience; blue carbon ecosystems; habitat fragmentation; spatiotemporal modeling; landscape connectivity; ecosystem services
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We welcome contributions for our upcoming Special Issue, “Allergic Diseases: Molecular Pathways and Pathogenesis”. This Special Issue will provide an in-depth exploration of the molecular mechanisms and pathogenesis underlying allergic diseases, focusing on the fundamental molecular pathways that drive allergic responses. Allergic diseases, such as asthma, rhinitis, atopic dermatitis, and food allergies, represent a growing global health concern, and understanding their molecular bases is crucial in order to advance treatment strategies.

This Special Issue will highlight cutting-edge research investigating the molecular pathways and immune mechanisms involved in allergic inflammation. We invite studies examining the roles of immune cells (such as T-helper cells, mast cells, and eosinophils), cytokines, and chemokines in the initiation and progression of allergic responses. This Special Issue will also explore the role of IgE-mediated responses and how they contribute to the pathology of allergic diseases. We encourage contributions that focus on genetic and epigenetic factors influencing allergic disease susceptibility, such as genetic mutations, epigenetic modifications, and non-coding RNAs. Furthermore, this Special Issue will examine the impacts of environmental exposures, such as allergens, pollutants, and microbiome alterations, in the development and exacerbation of allergic diseases.

This Special Issue will also highlight emerging biomarkers for early diagnosis and new therapeutic approaches, with a focus on precision medicine and targeted interventions for allergic diseases. We aim to integrate molecular, cellular, and clinical perspectives to foster a deeper understanding of the mechanisms driving allergic diseases and to contribute to the development of more effective treatments.

We invite original research articles, reviews, and perspectives that address the following themes:

  1. Molecular Mechanisms Behind Allergic Inflammation: Research investigating the cellular and molecular pathways involved in allergic inflammation, focusing on immune cells (e.g., T-helper cells, mast cells, eosinophils), cytokines, and chemokines;
  2. IgE-Mediated Responses: Studies exploring the role of IgE in allergic diseases, including its interactions with allergens and its contribution to allergic inflammation and immune response regulation;
  3. Genetic and Epigenetic Factors in Allergic Disease Susceptibility: Contributions exploring the genetic and epigenetic mechanisms that influence the onset and severity of allergic diseases, including non-coding RNAs;
  4. Environmental Exposures and Microbiome: Research on how environmental factors, including allergens, pollutants, and microbiome alterations, shape allergic disease pathogenesis and influence disease progression;
  5. Emerging Biomarkers and Therapeutic Strategies: Investigations into new biomarkers for diagnosis and innovative therapeutic approaches, with an emphasis on precision medicine and targeted therapies.

Submissions are encouraged from researchers across all relevant disciplines, including immunology, molecular biology, genetics, and environmental science. We look forward to receiving contributions that enhance our understanding of allergic diseases from a molecular and pathogenesis perspective.

Kind regards,

Dr. Jing Gao
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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology 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 2400 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

  • allergic diseases
  • allergic responses
  • allergic inflammation
  • immune response
  • genetics and susceptibility

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Published Papers (2 papers)

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Research

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18 pages, 2186 KB  
Article
Clinical Efficacy of TM02® in Allergic Rhinitis: Significant Symptom Alleviation Associated with IL-5 Downregulation and Reduced Allergic Inflammation
by Hao-Dong Tan, Sien-Hui Tan, Boon-Hong Kong, Chee-Kuan Wong, Revadi Govindaraju, Tengku Ahmad Shahrizal Tengku Omar and Shin-Yee Fung
Curr. Issues Mol. Biol. 2026, 48(9), 898; https://doi.org/10.3390/cimb48090898 - 2 Sep 2026
Viewed by 283
Abstract
Allergic rhinitis (AR) is a chronic inflammatory disease that substantially affects quality of life. Despite available therapies, symptom control remains suboptimal owing to treatment burden. Cultivated sclerotium of Lignosus rhinocerus (TM02®), known for its allergy-dampening bioactivities, is a promising adjunctive AR [...] Read more.
Allergic rhinitis (AR) is a chronic inflammatory disease that substantially affects quality of life. Despite available therapies, symptom control remains suboptimal owing to treatment burden. Cultivated sclerotium of Lignosus rhinocerus (TM02®), known for its allergy-dampening bioactivities, is a promising adjunctive AR treatment. A randomized, double-blinded clinical trial was conducted in 108 AR patients, who received either TM02® or placebo for 30 days. Primary outcomes consisted of Total Nasal Symptom Score (TNSS), reflective of past 12 h and 2 weeks (TNSS12hrs and TNSS2wks), and the Allergic Rhinitis Control Test (ARCT). The secondary endpoints were the peripheral immune biomarkers: IgE, IFNγ, IL-4, IL-5 and IL-13. Safety was assessed with adverse events (AEs) and full blood-counting analyses. Statistical analysis was performed using generalized estimating equation (GEE) in the modified per-protocol (mPP). mPP analysis (N_TM02® = 25; N_placebo = 31) demonstrated significant treatment effectiveness of TM02® in total TNSS12hrs, total TNSS2wks, and ARCT (β = −3.70, p-value < 0.001; β = −4.44, p-value < 0.001; and β = 3.89, p-value = 0.017, respectively). Secondary endpoint analysis did not reveal significant changes. However, a positive associative pattern (β = 14.94; p-value = 0.003) was observed between TNSS2wks and IL-5 level changes. There were no significant differences in AE incidences and laboratory safety biomarkers between treatment arms. The present study revealed that TM02® reduced AR symptom severity with minimal adverse effects. The underlying mechanism may involve the modulation of IL-5 levels and allergic inflammation. Overall, TM02® is a potential adjunctive or complementary treatment option for AR with persistent symptoms. Full article
(This article belongs to the Special Issue Allergic Diseases: Molecular Pathways and Pathogenesis)
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Review

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31 pages, 383 KB  
Review
Narrative Review of the Role of Reactive Oxygen Species in Allergic Rhinitis
by Jeongmin Lee, Su Young Jung, Hye Ok Kim, Jae Min Lee, Manish Kumar Singh, Sung Soo Kim, Jeon Gang Doo and Seung Geun Yeo
Curr. Issues Mol. Biol. 2026, 48(9), 947; https://doi.org/10.3390/cimb48090947 - 16 Sep 2026
Abstract
Studies of allergic rhinitis (AR) have increasingly recognized that reactive oxygen species (ROS) are not simply byproducts of oxidative metabolism but function as modulators of the type 2 inflammatory network during the pathogenesis of this disease. This narrative review summarizes the role of [...] Read more.
Studies of allergic rhinitis (AR) have increasingly recognized that reactive oxygen species (ROS) are not simply byproducts of oxidative metabolism but function as modulators of the type 2 inflammatory network during the pathogenesis of this disease. This narrative review summarizes the role of ROS in the pathophysiology of AR by analyzing studies that examined markers of systemic oxidative stress, dysfunction of the epithelial barrier, ROS derived from immune cells, mitochondrial redox signaling, and inflammasome-related pathways. Our structured search of the literature reviewed five major databases (PubMed, Scopus, EMBASE, Cochrane Library, and Google Scholar) and identified 17 eligible studies published between 2000 and 2026. Clinical studies suggest that patients with AR exhibit altered systemic redox homeostasis, including thiol–disulfide imbalance and increased lipid peroxidation. However, these findings are primarily from measurements of markers in peripheral blood, not nasal mucosa. Experimental studies consistently demonstrated that allergen exposure increased the levels of ROS in nasal epithelial and immune cells, disrupted the epithelial barrier, downregulated tight junction proteins, and activated inflammatory signaling pathways. Although direct nasal tissue data remain limited, evidence extrapolated from peripheral blood and bronchial challenge models suggests that eosinophils and neutrophils contribute to the generation of ROS during the late phase of the allergic response, thereby potentially amplifying and sustaining airway inflammation. There is also evidence that mitochondrial ROS and DUOX-dependent signaling contribute to epithelial dysfunction, including the release of damage-associated molecular patterns and activation of inflammasome pathways. In parallel, antioxidant defense mechanisms, such as the KEAP1/NRF2 axis and mitophagy-related pathways, appear to modulate disease severity by maintaining redox homeostasis. Experimental strategies such as ROS scavengers and oxidative stress-responsive drug delivery systems have shown early proof-of-concept potential in preclinical and pilot studies, but rigorous and large-scale clinical support is strictly required before any clinical application can be considered. Overall, current evidence indicates that ROS function in AR as context-dependent redox mediators rather than as primary causes. The biological effects of ROS appear to depend on site of synthesis, subcellular localization, and the balance between oxidant generation and antioxidant defenses. Further studies that directly assess the dynamics of nasal mucosal ROS and well-designed clinical trials are needed to clarify the translational relevance of these studies and the therapeutic potential of different treatments for AR. Full article
(This article belongs to the Special Issue Allergic Diseases: Molecular Pathways and Pathogenesis)
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