Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
4.9
Journals
IJMS
Special Issues
Advances in the Pathogenesis of Allergic Diseases: From Mechanisms to...
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Advances in the Pathogenesis of Allergic Diseases: From Mechanisms to Therapeutics

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 December 2025 | Viewed by 1031

Special Issue Editors

Dr. Clinton B. Mathias

E-Mail Website
Guest Editor
Department of Nutritional Sciences, University of Connecticut, Mansfield, CT, USA
Interests: mast cells; food allergy; allergic diseases
Dr. Michiko K. Oyoshi

E-Mail Website
Guest Editor
Massachusetts General Hospital, Boston, MA, USA
Interests: food allergy; mast cells; allergic diseases

Special Issue Information

Dear Colleagues,

Allergic Diseases such as food allergy and allergic asthma are a growing public health concern, affecting one-third of the American population and on the rise in urban areas globally. Recent research has uncovered various endogenous and environmental factors that contribute to the development of allergic disease, including genetic variations, epigenetic modifications, immune dysregulation, dietary components, the gut microbiome, and dietary patterns and habits. These factors not only regulate the intensity of allergic sensitization but also amplify the immune response to harmless, innocuous environmental allergens. Moreover, groundbreaking discoveries in immune cell mechanisms and functions have significantly advanced our understanding of allergy pathogenesis, shedding light on the roles of various cells and proteins, such as T and B cells, mast cells, group 2 innate lymphoid cells, and eosinophils, as well as cytokines like IL-33, IL-25, TSLP, and IL-4 and IL-13. These findings have paved the way for the development of novel therapeutic approaches that target these pathways and mediators.

In this issue, we are delighted to welcome original research and review articles that further enrich the existing literature on the mechanisms underlying the pathogenesis of allergic diseases and the development of therapeutic approaches.

Dr. Clinton B. Mathias
Dr. Michiko K. Oyoshi
Guest Editors

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

  • food allergy
  • allergic mechanisms
  • asthma
  • allergic disease
  • mast cells
  • ILC2s
  • Th2 cells
  • eosinophils
  • IL-4
  • IL-33
  • IL-13

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

15 pages, 1785 KiB  
Article
Paradoxical Use of Benralizumab in Reactive Hypereosinophilia from Toxocariasis and Tuberculosis Co-Infection—Case Report and Literature Review
by Nicoleta Sorina Bertici, Talida Georgiana Cut, Amalia Ridichie, Andrei Raul Manzur and Razvan Adrian Bertici
Int. J. Mol. Sci. 2025, 26(17), 8117; https://doi.org/10.3390/ijms26178117 - 22 Aug 2025
Abstract
Tuberculosis and parasitic infections, including Toxocara, frequently coexist in many regions worldwide, yet their interaction remains poorly understood. Tuberculosis triggers a type 1 immune response characterized by IL-12, IFN-γ, and TNF-α production, while toxocariasis elicits a type 2 response, mediated by cytokines [...] Read more.
Tuberculosis and parasitic infections, including Toxocara, frequently coexist in many regions worldwide, yet their interaction remains poorly understood. Tuberculosis triggers a type 1 immune response characterized by IL-12, IFN-γ, and TNF-α production, while toxocariasis elicits a type 2 response, mediated by cytokines such as IL-4, IL-5, IL-13, and IL-33. The coexistence of these divergent immune pathways can disrupt immune regulation and impair the host’s ability to control both infections, potentially leading to persistent hypereosinophilia. We illustrate this complex interplay through a real-world case involving a heavy smoker in whom Toxocara infection likely reactivated latent tuberculosis, resulting in severe, unexplained hypereosinophilia and late-onset asthma with recurrent exacerbations. After excluding other causes and completing full antituberculosis therapy along with three courses of antiparasitic treatment and systemic corticosteroids, hypereosinophilia persisted. The introduction of benralizumab, a biologic therapy targeting IL-5Rα, led to a rapid reduction in eosinophils to normal ranges and significant clinical improvement. This case underscores the diagnostic and therapeutic challenges posed by the intersection of common infections and highlights that even a neglected parasitic infection such as toxocariasis can underlie severe respiratory complications with eosinophilia, where paradoxically biologic therapy may ultimately provide a very effective intervention. Full article
(This article belongs to the Special Issue Advances in the Pathogenesis of Allergic Diseases: From Mechanisms to Therapeutics)
►▼ Show Figures

Figure 1

15 pages, 6242 KiB  
Article
IgG:FcγRIIb Signaling on Mast Cells Blocks Allergic Airway Inflammation
by Cynthia Kanagaratham, Yasmeen S. El Ansari, Kameryn N. Furiness and Hans C. Oettgen
Int. J. Mol. Sci. 2025, 26(14), 6779; https://doi.org/10.3390/ijms26146779 - 15 Jul 2025
Viewed by 399
Abstract
IgG antibodies, signaling via the inhibitory receptor, FcγRIIb, are potent inhibitors of IgE-mediated mast cell activation. We have previously reported that in addition to blocking mast cell degranulation, inhibitory IgG signals shut down a proinflammatory transcriptional program in which mast cells produce cytokines [...] Read more.
IgG antibodies, signaling via the inhibitory receptor, FcγRIIb, are potent inhibitors of IgE-mediated mast cell activation. We have previously reported that in addition to blocking mast cell degranulation, inhibitory IgG signals shut down a proinflammatory transcriptional program in which mast cells produce cytokines and chemokines known to drive type 2 tissue inflammation. To determine whether such effects of allergen-specific IgG can modulate allergic inflammation in vivo, we examined the airways of mice sensitized to ovalbumin (OVA) by intraperitoneal injection and then challenged with intranasal OVA. Pretreatment with allergen-specific IgG significantly reduced the recruitment of inflammatory cells, including macrophages and eosinophils, into the lungs of OVA-sensitized mice. The bronchoalveolar lavage fluid of OVA-challenged mice contained elevated levels of chemokine ligands (CCL2 and CCL24) and interleukin-5, a response that was markedly blunted in animals receiving allergen-specific IgG. IgG-treated animals exhibited attenuated allergen-induced production of IgE, IL-4, and IL-13, along with impaired OVA-induced goblet cell hyperplasia and Muc5ac expression and suppressed airway hyperresponsiveness, consistent with a shift away from a Th2 response. Using mice with a lineage-specific deletion of FcγRIIb, we demonstrated that each of these protective effects of IgG was dependent upon the expression of this receptor on mast cells. Overall, our findings establish that allergen-specific IgG can reduce allergen-driven airway inflammation and airway hyperresponsiveness and point to a mechanistic basis for the therapeutic benefit of aeroallergen-specific IgG therapy. Full article
(This article belongs to the Special Issue Advances in the Pathogenesis of Allergic Diseases: From Mechanisms to Therapeutics)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop