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9.2
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Journals
Biomolecules
Special Issues
Molecular Basis of Mast Cells Activation and Medical Implications
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Molecular Basis of Mast Cells Activation and Medical Implications

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 462

Special Issue Editors

Dr. Grzegorz Porebski

E-Mail Website
Guest Editor
Department of Clinical and Environmental Allergology, Jagiellonian University Medical College, 31-503 Krakow, Poland
Interests: mast cell; immediate hypersensitivity; drug allergy; hereditary angioedema; C1 inhibitor deficiency
Dr. Matija Rijavec

E-Mail Website
Guest Editor
Laboratory for Clinical Immunology and Molecular Genetics, University Clinic of Respiratory and Allergic Diseases, 4204 Golnik, Slovenia
Interests: basophils; Hymenoptera venom anaphylaxis; mast cell disorders; hereditary alpha-tryptasemia; hereditary angioedema
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mast cells respond to environmental cues and inflammatory signals. This response translates into complex roles in immunity, tissue homeostasis, and diseases, particularly allergy and hypersensitivity reactions. They are activated through various receptors, including the high-affinity IgE receptor, cytokine receptors, and pattern recognition receptors. Subsequently, intracellular signaling pathways and calcium signaling events lead to mast cell degranulation, mediator release, and the development of a wide range of immediate hypersensitivity medical conditions, from local urticaria to anaphylaxis.

Over the last decade, significant progress has been made in understanding mast cell activation and the regulation mechanisms that may be involved in the development and progression of allergy and hypersensitivity reactions.

The aim of this Special Issue is to highlight recent advances in this field, which may be useful in the prevention of individuals of developing immediate hypersensitivity reactions and in the development of pharmacotherapeutic strategies through the evaluation of novel effective molecular targets.

We encourage researchers who are interested in this topic to submit original research articles that highlight the current preclinical and clinical knowledge on the molecular basis of mast cell activation and implications for the development of mast-cell-driven allergy and hypersensitivity reactions. In addition, critical and systematic review articles covering the relevant research, with concluding remarks and suggestions for future work, will also be considered for inclusion in this Special Issue.

Dr. Grzegorz Porebski
Dr. Matija Rijavec
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. Biomolecules 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 2700 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

  • mast cells
  • allergy
  • immediate hypersensitivity
  • molecular mechanisms

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Published Papers (1 paper)

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Research

14 pages, 2287 KB  
Article
Icatibant Acts as a Balanced Ligand of MRGPRX2 in Human Skin Mast Cells
by Zhuoran Li, Jean Schneikert, Gürkan Bal, Torsten Zuberbier and Magda Babina
Biomolecules 2025, 15(9), 1224; https://doi.org/10.3390/biom15091224 (registering DOI) - 25 Aug 2025
Abstract
MRGPRX2 (Mas-related G protein-coupled receptor member X2) is implicated in mast cell (MC)-driven disorders due to its ability to bind diverse ligands, which may be G-protein-biased or balanced, with the latter activating both G-proteins and the β-arrestin pathway. Icatibant, a peptide drug, produces [...] Read more.
MRGPRX2 (Mas-related G protein-coupled receptor member X2) is implicated in mast cell (MC)-driven disorders due to its ability to bind diverse ligands, which may be G-protein-biased or balanced, with the latter activating both G-proteins and the β-arrestin pathway. Icatibant, a peptide drug, produces injection-site reactions in most patients and is used experimentally to probe MRGPRX2 function in skin tests. While reported to be G-protein-biased, it is unknown how skin MCs respond to icatibant, although these are the primary target cells during therapy. We therefore compared responses to icatibant with those induced by the balanced agonist substance P (SP) in skin MCs. Degranulation and desensitization were assessed via β-hexosaminidase release, receptor internalization by flow cytometry, and downstream signaling by immunoblotting. Skin MCs degranulated in response to SP and icatibant, relying on Gi proteins and calcium channels; Gq and PI3K (Phosphoinositide 3-kinase) contributed more strongly to exocytosis following icatibant, while JNK (c-Jun n-terminal kinase) was more relevant for SP. Both agonists activated ERK, PI3K/AKT, and (weakly) p38. Surprisingly, and in contrast to the LAD2 (Laboratory of Allergic Diseases 2 mast cell line) MC line, icatibant was at least as potent as SP in eliciting MRGPRX2 internalization and (cross-)desensitization in skin MCs. These findings suggest that icatibant functions differently in primary versus transformed MCs, acting as a fully balanced ligand in the former by triggering not only degranulation but also receptor internalization and desensitization. Therefore, not only the ligand but also the MRGPRX2-expressing cell plays a decisive role in whether a ligand is balanced or biased. These findings are relevant to our understanding of icatibant’s clinical effects on edema and itch. Full article
(This article belongs to the Special Issue Molecular Basis of Mast Cells Activation and Medical Implications)
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