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Cells
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Mast Cells in Health and Disease: Current Insights and Future...
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Mast Cells in Health and Disease: Current Insights and Future Perspectives on Development, Activation, Functional Roles, and Therapeutic Strategies

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: 15 April 2026 | Viewed by 3879

Special Issue Editor

Dr. Aida Paivandy

E-Mail Website
Guest Editor
Department of Medical Sciences, Uppsala University, Uppsala, Sweden
Interests: mast cells; mast cell proteases; inflammation; allergy; asthma; chronic obstructive pulmonary disease (COPD); autoimmune disorders; therapeutic innovations; cellular stress; apoptosis; multi-omics analysis

Special Issue Information

Dear Colleagues,

Mast cells (MCs) are multifaceted effector cells of the immune system, characterized by their abundance of secretory granules packed with a variety of bioactive mediators, including histamine, cytokines, and MC-specific proteases. These cells are widely distributed throughout the body, with higher abundance in tissues that serve as entry points for external insults, and are equipped with a broad range of sensing receptors. Upon recognition of stimuli via their receptors, MCs become activated and release a panel of inflammatory mediators, allowing them to orchestrate inflammation and play a key role in host defense against microbial pathogens and poisonous substances. However, dysregulated MC activation can contribute to the pathogenesis of various diseases, in particular allergic conditions, including asthma and atopic dermatitis, as well as other pathological conditions, such as cutaneous mastocytosis, fibrosis, cancer and autoimmune disorders. Therefore, strategies targeting MCs hold significant promise for treating these diseases. Potential approaches include targeting individual MC mediators, blocking receptors for MC-released compounds, inhibiting MC activation, limiting MC growth, and reducing MC numbers through the induction of their apoptosis. Despite extensive research, the full spectrum of mast cells' pathophysiological roles remains incompletely understood.

In this Special Issue of Cells, we are inviting contributions, either in the form of original research articles, reviews, or shorter perspective articles on all aspects related to the theme of “Mast Cells in Health and Disease: Current Insights and Future Perspectives on Development, Activation, Functional Roles, and Therapeutic Strategies”. Articles with mechanistic and functional insights into cell and molecular biology, or in vivo studies are especially welcome. Relevant topics include, but are not limited to, the following:

  • Mast cell development and survival ;
  • Mast cell heterogeneity and plasticity;
  • Mast cell activation via IgE-dependent and -independent pathways;
  • Receptor signaling and signal transduction pathways governing mast cell activation and inhibition;
  • Mast cell mediators, their regulation and biological impacts;
  • Roles of mast cells in immunity and host defense against pathogens and toxins;
  • Mast cell roles in homeostasis and tissue repair;
  • Mast cell roles in the pathogenesis of allergic and non-allergic inflammatory diseases;
  • Emerging detrimental effects of mast cells and their contribution to diverse pathological conditions;
  • Contribution of mast cell-specific mediators (e.g., tryptase, chymase, and carboxypeptidase A3) to disease progression and physiological function;
  • Mast cell communication and interaction with immune and non-immune cells;
  • In vivo models to investigate mast cell pathophysiological functions;
  • Advanced techniques for studying mast cell biology (e.g., single-cell analysis, in vivo imaging);
  • Novel therapeutic approaches targeting mast cells and their mediators.

Dr. Aida Paivandy
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. Cells is an international peer-reviewed open access semimonthly 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 cell granules
  • mast cell mediators
  • mast cell development
  • mast cell survival
  • mast cell activation
  • mast cell activating and inhibitory receptors
  • receptor signaling
  • allergic and non-allergic pathologies
  • immunity and host defense
  • mast cell-directed therapeutic approaches

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Published Papers (4 papers)

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Research

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24 pages, 3826 KB  
Article
Spatial Phenotype of the Mast Cell Population in Endometritis of Various Severities
by Sergey Mikhalev, Andrey Kostin, Mark Kurtser, Victor Radzinsky, Mekan Orazov, Alexander Alekhnovich, Aleksandra Prikhodko, Grigory Demyashkin, Ilya Klabukov, Denis Baranovskii, Daniel Elieh-Ali-Komi, Igor Buchwalow, Markus Tiemann, Liudmila Mikhaleva and Dmitrii Atiakshin
Cells 2026, 15(1), 38; https://doi.org/10.3390/cells15010038 - 24 Dec 2025
Viewed by 502
Abstract
Endometritis features an inflammatory milieu in the endometrium, accompanied by the recruitment of immunocompetent cells, including mast cells (MCs). The mechanisms underlying MC involvement in chronic endometritis (CE) and fibrous niche formation remain poorly understood, particularly regarding spatial intercellular interactions in situ. In [...] Read more.
Endometritis features an inflammatory milieu in the endometrium, accompanied by the recruitment of immunocompetent cells, including mast cells (MCs). The mechanisms underlying MC involvement in chronic endometritis (CE) and fibrous niche formation remain poorly understood, particularly regarding spatial intercellular interactions in situ. In this study, we used multiplex immunohistochemistry and quantitative immunofluorescence analysis to map the spatial phenotype of MC distribution. Standard histochemical techniques, monoplex and multiplex immunohistochemical staining technologies, light-field microscopy, epifluorescence, and confocal microscopy with multispectral imaging, combined with quantitative immunofluorescence analysis with AI application, were used to identify the spatial phenotyping of quantitative and qualitative features of the endometrial MC population in CE. The increased intensity of endometrial inflammation was accompanied by a rise in the profile of MC content in the endometrium; this accounted for a 0.014% increase in the control and 0.067%, 0.113%, and 0.206% increases in mild, moderate, and severe CE, respectively. We are the first to map the number of MCs that demonstrated loci of accumulations in the endometrium coinciding with foci of fibrous changes. The number of these foci correlated with the severity of chronic endometritis and the development of clinical signs. The frequency of juxtacrine and paracrine MC colocalization with other immunocompetent cells increased with increased CE activity and fibrotic changes: For CD8+ lymphocytes, colocalization increased from 4.6% in the control to 11.6%, 18.5%, and 28.0% in mild, moderate, and severe CE, respectively. For monocytes, colocalization increased from 5.6% in the control to 18.7%, 26.8%, and 28.8% in mild, moderate, and severe CE, respectively. For type 1 macrophages, colocalization increased from 5.6% in the control to 13.5%, 17.4%, and 24.6% in mild, moderate, and severe CE, respectively. For type 2 macrophages, colocalization increased from 3.4% in the control to 9.6%, 9.1%, and 21.5% in mild, moderate, and severe CE, respectively. Spatial patterns of juxtacrine and paracrine MC interactions with other immune cells may provide diagnostic algorithms for chronic endometritis, enabling targeted therapy and preventing fibrotic changes. Full article
(This article belongs to the Special Issue Mast Cells in Health and Disease: Current Insights and Future Perspectives on Development, Activation, Functional Roles, and Therapeutic Strategies)
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17 pages, 1359 KB  
Article
Release of Mast Cell Mediators from Cochlear Tissue Following Short Exposure to Compound 48/80 or Cisplatin, and Their Damage to Cochlear Structure
by Bin Zeng, Stefan Frischbutter, Sherezade Moñino-Romero, Jörg Scheffel, Frank Siebenhaar, Heidi Olze and Agnieszka J. Szczepek
Cells 2025, 14(20), 1615; https://doi.org/10.3390/cells14201615 - 17 Oct 2025
Viewed by 792
Abstract
The cochlea is susceptible to damage from ototoxic agents such as cisplatin, yet the mechanisms underlying cochlear injury remain incompletely understood. Mast cells (MCs), key immune players in allergic and inflammatory responses, have recently been identified in the rodent cochlea and implicated in [...] Read more.
The cochlea is susceptible to damage from ototoxic agents such as cisplatin, yet the mechanisms underlying cochlear injury remain incompletely understood. Mast cells (MCs), key immune players in allergic and inflammatory responses, have recently been identified in the rodent cochlea and implicated in cisplatin-induced ototoxicity. Our study investigated the role of MC degranulation in cochlear damage and evaluated the activation capacity of cochlear-resident MCs. Bone marrow-derived MCs (BMMCs) were cultured and induced to degranulate via IgE-anti-DNP/DNP stimulation, and the supernatants were applied to cochlear explants. Cochlear explants were also treated with Compound 48/80 (CP48/80) or cisplatin to assess MC activation. Morphological changes were assessed and hair cells (HC) quantified via phalloidin staining, while ELISA measured mediator release. Supernatants from degranulated BMMC induced a dose-dependent HC loss and tissue damage. A significant chymase and tryptase release was triggered by CP48/80 from cochlear MCs, with chymase elevation detected even at low concentrations. Cochlear MCs were rapidly activated by cisplatin exposure, elevating chymase and histamine levels, and the effects were attenuated by the MC stabilizer sodium cromolyn. Notably, tryptase remained undetectable post-cisplatin treatment, suggesting tissue-specific MC responses. These findings establish MC degranulation as an early event in cisplatin-induced cochlear injury, mediated by chymase and histamine. Our study highlights MCs as potential therapeutic targets for mitigating ototoxicity and underscores the need to explore MC-driven pathways in hearing loss. Full article
(This article belongs to the Special Issue Mast Cells in Health and Disease: Current Insights and Future Perspectives on Development, Activation, Functional Roles, and Therapeutic Strategies)
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15 pages, 3122 KB  
Article
Ac2–26 Hydrogel Modulates IL-1β-Driven Inflammation via Mast Cell-Associated and Immune Regulatory Pathways in Diabetic Wounds
by Monielle Sant’Ana, Rafael André da Silva, Luiz Philipe S. Ferreira, Cristiane D. Gil, Fernando L. Primo, Ana Paula Girol, Karin V. Greco and Sonia M. Oliani
Cells 2025, 14(13), 999; https://doi.org/10.3390/cells14130999 - 30 Jun 2025
Cited by 1 | Viewed by 1313
Abstract
Chronic, non-resolving inflammation is a major contributor to impaired wound healing in diabetes. Annexin A1 (AnxA1), a pro-resolving mediator, and its mimetic peptide Ac2–26 have demonstrated therapeutic potential in modulating inflammatory responses. In this study, we evaluated the effects of topical Ac [...] Read more.
Chronic, non-resolving inflammation is a major contributor to impaired wound healing in diabetes. Annexin A1 (AnxA1), a pro-resolving mediator, and its mimetic peptide Ac2–26 have demonstrated therapeutic potential in modulating inflammatory responses. In this study, we evaluated the effects of topical Ac2–26 hydrogel in a streptozotocin-induced diabetic wound model. Treatment significantly accelerated wound closure, improved tissue architecture, and reduced leukocyte infiltration. Immunohistochemical analysis revealed diminished mast cell accumulation and IL-1β expression in treated wounds. Complementary transcriptomic profiling supported the downregulation of pro-inflammatory genes, including Il1b and mast cell-related mediators, confirming the peptide’s regulatory effect on the wound immune landscape. Mounting evidence suggests that dysregulated mast cell activity plays a role in the heightened inflammatory tone and delayed tissue repair observed in diabetic wounds. In our model, Ac2–26 hydrogel treatment attenuated IL-1β expression, suggesting an indirect downregulation of NLRP3 inflammasome activation, potentially mediated through mast cell modulation, though effects on other cell types within the wound microenvironment cannot be excluded. While definitive causality cannot be assigned, the integration of histological and transcriptomic data highlights mast cells as contributors to the IL-1β-driven inflammatory burden in diabetic wounds. These findings underscore the immunomodulatory capacity of Ac2–26 and its potential to restore resolution pathways in chronic wound settings, positioning it as a promising candidate for future therapeutic development. Full article
(This article belongs to the Special Issue Mast Cells in Health and Disease: Current Insights and Future Perspectives on Development, Activation, Functional Roles, and Therapeutic Strategies)
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Review

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34 pages, 1420 KB  
Review
Skeletal Involvement in Systemic Mastocytosis: Pathophysiology, Clinical Management, Standards of Care, and Novel Therapeutic Strategies
by Manlio Fazio, Adele Bottaro, Maria Elisa Nasso, Fabio Stagno and Alessandro Allegra
Cells 2026, 15(3), 307; https://doi.org/10.3390/cells15030307 - 6 Feb 2026
Abstract
Systemic mastocytosis comprises a group of clonal mast cell disorders characterized by multisystem involvement. Bone involvement represents a major source of morbidity, particularly in young men affected by indolent systemic mastocytosis. This review provides an integrated and up-to-date overview of SM-related bone disease. [...] Read more.
Systemic mastocytosis comprises a group of clonal mast cell disorders characterized by multisystem involvement. Bone involvement represents a major source of morbidity, particularly in young men affected by indolent systemic mastocytosis. This review provides an integrated and up-to-date overview of SM-related bone disease. We dissect the dual and context-dependent role of mast cells in bone remodeling, detailing how they promote osteoclastogenesis, suppress osteoblast function, and, in advanced disease, drive osteosclerosis. We critically appraise available treatments, including classic anti-resorptive therapy and emerging anabolic strategies. We further discuss the transformative impact of KIT-directed tyrosine kinase inhibitors, particularly avapritinib, which has demonstrated for the first time the ability to reverse not only osteoporosis but also osteosclerosis. Finally, we explore the emerging role of machine learning models in SM, proposing their application to individualized prediction of osteoporosis and fracture risk in SM. By bridging clinical care, bone biology, and therapeutic advances, this review underscores the need for a paradigm shift in which SM-related bone disease is recognized as a dynamic process requiring early identification, integrated risk stratification, and coordinated use of anti-resorptive, disease-modifying, and data-driven precision approaches to prevent fractures and improve long-term outcomes and quality of life in this delicate category of patients. Full article
(This article belongs to the Special Issue Mast Cells in Health and Disease: Current Insights and Future Perspectives on Development, Activation, Functional Roles, and Therapeutic Strategies)
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