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 533

Special Issue Editor


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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

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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 (1 paper)

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Research

15 pages, 3122 KiB  
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
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
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