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Peer-reviewedCC BY-NC 4.0Journal of Inflammation Research

Key Players and Pathways of Mast Cell Activation in Urticaria

  • Carolin Jahn1,2
  • Dimitra Gialama1,2
  • Margarita Pashuk1,2,3
  • Yi-Kui Xiang1,2
  • Pavel Kolkhir1,2
  1. 1Insitiute of Allergology, Charité – University Medical Center Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institute of Allergology, Berlin, Germany
  2. 2Fraunhofer Institute for Translational Medicine and Pharmacology ITMP, Immunology and Allergology, Berlin, Germany
  3. 3Department of Biology, Chemistry and Pharmacy, Freie Universität Berlin, Berlin, Germany
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Abstract

Mast cells (MCs) are the principal effector cells in urticaria, orchestrating the release of mediators that drive wheal formation, angioedema, and pruritus. Although activation of MCs via the immunoglobulin (Ig) E and its high-affinity receptor (FcεRI) axis, including autoimmune urticaria mediated by IgE and IgG autoantibodies, remains the best characterized pathway, increasing evidence indicates that additional mechanisms contribute to disease pathogenesis. These include Mas-related G protein-coupled receptor X2 (MRGPRX2), c-Kit (key regulator of mast cell differentiation, proliferation, and survival), complement, coagulation, and the microbiome. Emerging data suggest that multiple pathways may coexist and interact within individual patients. Variability in the relative contribution and interaction of these pathways likely underlies the clinical heterogeneity of urticaria and the differences observed in therapeutic responses. Improved characterization of molecular endotypes and identification of reliable biomarkers, will be essential for advancing precision medicine in urticaria, especially as emerging therapies, including BTK, KIT, and JAK inhibitors, provide opportunities to selectively target distinct components of disease pathogenesis. This review provides an overview of key players, signaling pathways and molecular mechanisms involved in MC activation and degranulation in urticaria, focusing on chronic urticaria, especially chronic spontaneous urticaria.

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Cite

BibTeXRIS
BibTeX
@article{jahn2026players,
  title = {{Key Players and Pathways of Mast Cell Activation in Urticaria}},
  author = {Carolin Jahn and Dimitra Gialama and Margarita Pashuk and Yi-Kui Xiang and Pavel Kolkhir},
  journal = {Journal of Inflammation Research},
  year = {2026},
  month = oct,
  doi = {10.2147/jir.s589940},
  url = {https://doi.org/10.2147/jir.s589940},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - Key Players and Pathways of Mast Cell Activation in Urticaria
AU  - Carolin Jahn
AU  - Dimitra Gialama
AU  - Margarita Pashuk
AU  - Yi-Kui Xiang
AU  - Pavel Kolkhir
PY  - 2026
DA  - 2026/10/30
JO  - Journal of Inflammation Research
DO  - 10.2147/jir.s589940
UR  - https://doi.org/10.2147/jir.s589940
AB  - Mast cells (MCs) are the principal effector cells in urticaria, orchestrating the release of mediators that drive wheal formation, angioedema, and pruritus. Although activation of MCs via the immunoglobulin (Ig) E and its high-affinity receptor (FcεRI) axis, including autoimmune urticaria mediated by IgE and IgG autoantibodies, remains the best characterized pathway, increasing evidence indicates that additional mechanisms contribute to disease pathogenesis. These include Mas-related G protein-coupled receptor X2 (MRGPRX2), c-Kit (key regulator of mast cell differentiation, proliferation, and survival), complement, coagulation, and the microbiome. Emerging data suggest that multiple pathways may coexist and interact within individual patients. Variability in the relative contribution and interaction of these pathways likely underlies the clinical heterogeneity of urticaria and the differences observed in therapeutic responses. Improved characterization of molecular endotypes and identification of reliable biomarkers, will be essential for advancing precision medicine in urticaria, especially as emerging therapies, including BTK, KIT, and JAK inhibitors, provide opportunities to selectively target distinct components of disease pathogenesis. This review provides an overview of key players, signaling pathways and molecular mechanisms involved in MC activation and degranulation in urticaria, focusing on chronic urticaria, especially chronic spontaneous urticaria.
SN  - 1178-7031
ER  -