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Allergic Diseases: Molecular Insights into Immunotherapy

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 1585

Special Issue Editor


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Guest Editor
SCDU Immunologia e Allergologia, A.O. Ordine Mauriziano di Torino, C.so Re Umberto 109, 10128 Torino, Italy
Interests: asthma; allergy; clinical immunology; immunodeficiency; hypereosinophilic syndrome; urticaria; rhinitis; food allergy

Special Issue Information

Dear Colleagues,

We are pleased to announce the upcoming release of a Special Issue entitled “Allergic Diseases: Molecular Insights into Immunotherapy” in our journal. This Special Issue aims to provide a comprehensive overview of the latest advancements in the field of immunotherapy for allergic diseases, with a focus on molecular insights. Allergic diseases continue to pose a significant health burden globally, and immunotherapy has emerged as a promising treatment strategy. This Special Issue will feature original research articles, reviews, and clinical studies that explore the molecular mechanisms underlying immunotherapy for allergic diseases.

The topics covered in this Special Issue will include, but are not limited to, the role of specific immunotherapy in modulating immune responses, novel molecular targets for immunotherapy, personalized approaches to immunotherapy, and the use of biomarkers to predict treatment outcomes. Our goal is to provide allergists, immunologists, and other healthcare professionals with valuable insights into the molecular basis of immunotherapy for allergic diseases, ultimately advancing the development of more effective and targeted treatment options. We invite researchers and experts in the field to contribute their cutting-edge work to this Special Issue, fostering a deeper understanding of the molecular aspects of immunotherapy for allergic diseases.

Dr. Stefania Nicola
Guest Editor

Manuscript Submission Information

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Keywords

  • component resolved diagnosis
  • allergen immunotherapy
  • molecular diagnostic
  • basophil activation test
  • anaphylaxis
  • allergy diagnosis
  • in vitro tests
  • in vivo tests
  • skin prick test

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Published Papers (3 papers)

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Research

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12 pages, 1191 KiB  
Article
Ex Vivo Overactivation of Lymphocyte Subsets in Fibrotic Hypersensitivity Pneumonitis Is Blunted by a Sphingosine-1-Phosphate Receptor Ligand
by Olivier Courtemanche, Carole-Ann Huppé, Pascale Blais-Lecours, Cloé Maranda, Mathieu C. Morissette, Marie-Renée Blanchet, Geneviève Dion and David Marsolais
Int. J. Mol. Sci. 2025, 26(7), 3197; https://doi.org/10.3390/ijms26073197 - 29 Mar 2025
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Abstract
Lymphocytes are central to the pathogenesis of hypersensitivity pneumonitis and a strong body of evidence supports that lymphocytes are modulated by sphingosine-1-phosphate receptor-modifying drugs. This exploratory study aimed to determine if a pharmacological sphingosine-1-phosphate receptor ligand interfered with the activation of lymphocytes obtained [...] Read more.
Lymphocytes are central to the pathogenesis of hypersensitivity pneumonitis and a strong body of evidence supports that lymphocytes are modulated by sphingosine-1-phosphate receptor-modifying drugs. This exploratory study aimed to determine if a pharmacological sphingosine-1-phosphate receptor ligand interfered with the activation of lymphocytes obtained from fibrotic hypersensitivity pneumonitis patients. Peripheral blood mononuclear cells of 12 patients and 10 control subjects were submitted to CD3/CD28 stimulation, isolated B cells were incubated with a TLR9 ligand; and we tested how these stimulations were impacted by ozanimod, a sphingosine-1-phosphate receptor ligand. T cell and B cell subsets from patients overexpressed CD69 and cytokines such as TNF and IL-4 in response to CD3/CD28 stimulation, compared to controls. In patients with fibrotic hypersensitivity pneumonitis, ozanimod alleviated CD3/CD28 induction of CD69, IL-4, and TNF in CD8, but not CD4 T cells. In isolated B cells stimulated with a TLR9 ligand, ozanimod reduced cell surface expression of CD69, CD86, and CD40, as well as TNF and IL-6 accumulation in supernatant. We conclude that lymphocyte subsets are functionally impacted in patients with fibrotic hypersensitivity pneumonitis and that ozanimod can interfere ex vivo with the overactivation of B cells and CD8 T cells in response to specific stimuli. Full article
(This article belongs to the Special Issue Allergic Diseases: Molecular Insights into Immunotherapy)
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19 pages, 10777 KiB  
Article
Sensitization Potential of the Major Soybean Allergen Gly m 4 and Its Cross-Reactivity with the Birch Pollen Allergen Bet v 1
by Ekaterina I. Finkina, Yulia D. Danilova, Daria N. Melnikova, Tatiana V. Ovchinnikova and Ivan V. Bogdanov
Int. J. Mol. Sci. 2025, 26(7), 2932; https://doi.org/10.3390/ijms26072932 - 24 Mar 2025
Viewed by 383
Abstract
The birch pollen allergen Bet v 1 is believed to be the main sensitizer among PR-10 allergens. Recent data have shown that some other PR-10 allergens also display sensitization activities, and Bet v 1-based immunotherapy is not effective for blocking allergic reactions to [...] Read more.
The birch pollen allergen Bet v 1 is believed to be the main sensitizer among PR-10 allergens. Recent data have shown that some other PR-10 allergens also display sensitization activities, and Bet v 1-based immunotherapy is not effective for blocking allergic reactions to PR-10 proteins with low similarities to Bet v 1. Here, we investigated the sensitization potential of the major soybean allergen Gly m 4 and its cross-reactivity with Bet v 1. We demonstrated that Gly m 4 bound cholesterol and bile acids, including deoxycholic acid (DCA). Using qPCR, we showed that Gly m 4 induced the expression of genes encoding alarmins TSLP and IL-33 in intestinal-like Caco-2 cells; however, its fragments resulting from digestion by gastroduodenal enzymes or the DCA-bound Gly m 4 caused more pronounced gene upregulation. Using competitive ELISA, we demonstrated the low cross-reactivity of anti-Gly m 4 and anti-Bet v 1 IgG, raised in laboratory animals. Using mice allergy models with sensitization to birch or soybean allergens, we also showed a low cross-reactivity of Gly m 4- and Bet v 1-specific IgE, IgG1 and IgG2a. Thus, our findings support an assumption of the intrinsic sensitization capacity of Gly m 4 and the existence of Gly m 4-specific antibodies in sera of allergic patients. Full article
(This article belongs to the Special Issue Allergic Diseases: Molecular Insights into Immunotherapy)
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Review

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15 pages, 951 KiB  
Review
Allergen Immunotherapy: Pitfalls, Perks and Unexpected Allies
by Tudor Paul Tamaș and Elena Ciurariu
Int. J. Mol. Sci. 2025, 26(8), 3535; https://doi.org/10.3390/ijms26083535 - 9 Apr 2025
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Abstract
Allergen immunotherapy (AIT) is a well-established treatment aimed at reducing allergen sensitivity by gradually exposing the immune system to increasing doses of allergens. This promotes desensitization and immune tolerance through multiple mechanisms. AIT offers long-term immune modulation and is considered a potentially curative [...] Read more.
Allergen immunotherapy (AIT) is a well-established treatment aimed at reducing allergen sensitivity by gradually exposing the immune system to increasing doses of allergens. This promotes desensitization and immune tolerance through multiple mechanisms. AIT offers long-term immune modulation and is considered a potentially curative certain forms of allergic diseases. Altered antibody responses is a key mechanism of AIT in the production of allergen-specific IgG4 antibodies, which act as blocking antibodies to prevent allergen binding to IgE on mast cells (MCs) and basophils. However, IgG4 responses are sometimes ineffective due to variations in antibody affinity and epitope targeting. Reverse class switching from IgE to IgG4 and selective depletion of IgE-producing B cells represent potential strategies to improve AIT efficacy. Tregs play a central role in AIT by suppressing Th2-driven allergic responses and promoting immune tolerance through anti-inflammatory cytokines interleukin (IL)-10 and transforming growth factor (TGF)-β. However, genetic and environmental factors may impair Treg function, leading to AIT failure. AIT reduces MC and basophil activation, leading to long-term suppression of allergic inflammation. It modulates IgE-FcεRI interactions and cytokine signaling pathways, but in some cases, anaphylactic reactions or resistance to MC desensitization may occur. Discussion and conclusions: While AIT is a highly effective allergy treatment, variability in immune responses can impact its success. Advances in biologic therapies offer potential synergies with AIT. Understanding these interactions will help refine AIT strategies and improve patient outcomes. Full article
(This article belongs to the Special Issue Allergic Diseases: Molecular Insights into Immunotherapy)
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