Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (629 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Granulated cells that are found in almost all tissues, most abundantly in the skin and the gastrointestinal tract. Like the basophils, mast cells contain large amounts of histamine and heparin. Unlike basophils, mast cells normally remain in the tissues and do not circulate in the blood. Mast cells, derived from the bone marrow stem cells, are regulated by the stem cell factor.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Cell, Mast; Cells, Mast; Mast Cell; Basophils, Tissue; Basophil, Tissue; Tissue Basophil; Tissue Basophils.
Where it fits in the MeSH classification
- Broader topics
- Connective Tissue Cells; Immune System
Related concepts
Research landscape
PubMed indexes 32,624 records tagged with the MeSH heading “Mast Cells” (counts retrieved 2026-10-31). 3,771 of them (11.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 15,164 records.
Reviews account for 4,675 records (14.3%) and meta-analyses for 24. Randomized controlled trials number 173 (0.5%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 15,164 |
| 2000-2009 | 6,809 |
| 2010-2019 | 6,880 |
| 2020 onward | 3,771 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 4,675 | 14.3% |
| Meta-analyses | 24 | 0.1% |
| Randomized controlled trials | 173 | 0.5% |
Method: PubMed query "Mast Cells"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| A single-cell spatial chart of the airway wall reveals proinflammatory cellular ecosystems and their interactions in health and asthma | 2025 | Research article Design not recorded in structured metadata | 38 | cc by PMID 40399607 · DOI · PMC12133579 |
| A mast cell receptor mediates post-stroke brain inflammation via a dural-brain axis | 2025 | Research article Design not recorded in structured metadata | 33 | cc by PMID 40712576 · DOI · PMC12313293 |
| Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens | 2025 | Research article Design not recorded in structured metadata | 29 | cc by PMID 40773543 · DOI · PMC12513082 |
| Mast cell-expressed Mrgprb2/MRGPRX2 mediates gout pain and inflammation via a neuroimmune axis | 2026 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41574611 · DOI · PMC12892919 |
A single-cell spatial chart of the airway wall reveals proinflammatory cellular ecosystems and their interactions in health and asthma [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Determining spatial location of cells within tissues gives vital insight into the interactions between resident and inflammatory cells and is a critical factor for uncoupling the mechanisms driving disease.
- Closing excerpt
- This study provides an unprecedented view of the topography of the airway wall, revealing distinct, specific ecosystems within spatial niches to target for therapeutic intervention.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (154 words)
Determining spatial location of cells within tissues gives vital insight into the interactions between resident and inflammatory cells and is a critical factor for uncoupling the mechanisms driving disease. Here, we apply single-cell spatial transcriptomics to reveal the airway wall landscape in health and during asthma. We identified proinflammatory cellular ecosystems that exist within discrete spatial niches in healthy and asthma samples. These cellular hubs are characterized by a high level of chemokine and alarmin expression, along with unique combinations of stromal cells. Mechanistically, we demonstrated that receptors, such as ACKR1, retain immune mediators locally, while amphiregulin-expressing mast cells are prominent within these proinflammatory hubs. Despite anti-inflammatory treatments, the asthma airway mucosa exhibited a distinct remodeling program within these cellular ecosystems, marked by increased proximity between key cell types. This study provides an unprecedented view of the topography of the airway wall, revealing distinct, specific ecosystems within spatial niches to target for therapeutic intervention.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40399607 · DOI · PMC12133579
A mast cell receptor mediates post-stroke brain inflammation via a dural-brain axis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The immune environment surrounding the brain plays a fundamental role in monitoring signs of injury.
- Closing excerpt
- Collectively, our study identifies Mrgprb2 as a critical meningeal gatekeeper for immune migration from skull bone marrow reservoirs into the brain.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (151 words)
The immune environment surrounding the brain plays a fundamental role in monitoring signs of injury. Insults, including ischemic stroke, can disrupt this balance and incite an exaggerated inflammatory response, yet the underlying mechanism remains unclear. Here, we show that the mast-cell-specific receptor Mrgprb2 regulates post-stroke brain inflammation from the meninges. Mrgprb2 causes meningeal mast cell degranulation after stroke, releasing immune mediators. This process recruits skull bone marrow neutrophils into the dura and further promotes neutrophil migration from the dura into the brain by cleaving the chemorepellent semaphorin 3a. We demonstrate that the human ortholog, MRGPRX2, is expressed in human meningeal mast cells and is activated by upregulation of the neuropeptide substance P following stroke. Pharmacologically inhibiting Mrgprb2 reduces post-stroke inflammation and improves neurological outcomes in mice, providing a druggable target. Collectively, our study identifies Mrgprb2 as a critical meningeal gatekeeper for immune migration from skull bone marrow reservoirs into the brain.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40712576 · DOI · PMC12313293
Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Anaphylaxis is a life-threatening complication of food allergen exposure.
- Closing excerpt
- Mice genetically deficient in cysteinyl leukotriene synthesis, or those treated with the arachidonate 5-lipoxygenase (aLOX5) antagonist zileuton, were protected from oral antigen-induced responses, whereas those elicited by intravenous injection were unaltered.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (131 words)
Anaphylaxis is a life-threatening complication of food allergen exposure. Although mechanisms governing anaphylaxis after intravenous injection are defined in mice, these models neglect mucosal exposure that accompanies ingestion. We investigated the role of mast cells within the intestine of mice and found that oral anaphylaxis required immunoglobulin E-Fcε receptor 1 (IgE-FcεR1) signaling. Intestinal mast cells were a heterogeneous population, shaped by epithelial cues. Compared with connective tissue mast cells found throughout the body, intestinal mast cells largely resided in the epithelium, displayed divergent transcriptomes and effector functions, and had a diminished ability to generate histamine, but they enhanced leukotriene synthesis. Mice genetically deficient in cysteinyl leukotriene synthesis, or those treated with the arachidonate 5-lipoxygenase (aLOX5) antagonist zileuton, were protected from oral antigen-induced responses, whereas those elicited by intravenous injection were unaltered.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40773543 · DOI · PMC12513082
Mast cell-expressed Mrgprb2/MRGPRX2 mediates gout pain and inflammation via a neuroimmune axis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Acute severe joint pain is a major symptom in gouty arthritis (GA), and its adequate treatment represents an unmet medical need.
- Closing excerpt
- These findings suggest that synovial mast cell-expressed Mrgprb2/MRGPRX2 merits consideration as a key neuroimmune player and a potential therapeutic target for treating GA pain and joint inflammation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (193 words)
Acute severe joint pain is a major symptom in gouty arthritis (GA), and its adequate treatment represents an unmet medical need. Mrgprb2, a specific mast cell receptor, has been implicated in the generation of chronic pain by mobilizing mast cell degranulation, yet its significance in GA pain and joint inflammation is still not well defined. Here, we found that Mrgprb2 was expressed in mouse synovial mast cells. In a murine model of GA, acute blockade or genetic deletion of Mrgprb2 significantly attenuated arthritis pain and hyperexcitability of joint nociceptors with significant reductions in innate immune cell recruitment in the synovium. Under naive conditions, activation of synovial Mrgprb2 was sufficient to excite peripheral terminals of joint nociceptors to induce acute joint hypernociception via the mobilization of mast cell degranulation. Additionally, the level of the neuropeptide substance P (SP) was elevated in the synovium of GA model mice. Using humanized MRGPRX2-knockin mice, we revealed that SP contributed to joint pain and inflammation by activating mast cells through Mrgprb2/MRGPRX2. These findings suggest that synovial mast cell-expressed Mrgprb2/MRGPRX2 merits consideration as a key neuroimmune player and a potential therapeutic target for treating GA pain and joint inflammation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41574611 · DOI · PMC12892919
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Mast cells as sources of cytokines, chemokines, and growth factors [5]
- Research article The Role of Histamine and Histamine Receptors in Mast Cell-Mediated Allergy and Inflammation: The Hunt for New Therapeutic Targets [6]
- Research article Mast Cells in Inflammation and Disease: Recent Progress and Ongoing Concerns [7]
- Research article Role of Mast Cells in Shaping the Tumor Microenvironment [8]
- Research article Mast Cell Biology at Molecular Level: a Comprehensive Review [9]
- Research article Mast cell-neural interactions contribute to pain and itch [10]
References
- Joulia R, Patti S, Traves WJ, Loewenthal L, Yates L, Walker SA, et al.. A single-cell spatial chart of the airway wall reveals proinflammatory cellular ecosystems and their interactions in health and asthma. . 2025. PMID 40399607 · DOI · PMC12133579
- Kothari R, Abdulrahim MW, Oh HJ, Capuzzi DH, Kilgore CB, Nair SK, et al.. A mast cell receptor mediates post-stroke brain inflammation via a dural-brain axis. . 2025. PMID 40712576 · DOI · PMC12313293
- Bachtel ND, Cullen JL, Liu M, Erickson SA, Kutyavin VI, El-Naccache DW, et al.. Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens. . 2025. PMID 40773543 · DOI · PMC12513082
- Yang L, Liu C, Xiao J, Song Y, Chen H, Li D, et al.. Mast cell-expressed Mrgprb2/MRGPRX2 mediates gout pain and inflammation via a neuroimmune axis. . 2026. PMID 41574611 · DOI · PMC12892919
- Mukai K, Tsai M, Saito H, Galli SJ. Mast cells as sources of cytokines, chemokines, and growth factors. Immunol Rev. 2018. PMID 29431212 · DOI · PMC5813811
- Thangam EB, Jemima EA, Singh H, Baig MS, Khan M, Khan M, et al.. The Role of Histamine and Histamine Receptors in Mast Cell-Mediated Allergy and Inflammation: The Hunt for New Therapeutic Targets. Front Immunol. 2018. PMID 30150993 · DOI · PMC6099187
- Galli SJ, Gaudenzio N, Tsai M. Mast Cells in Inflammation and Disease: Recent Progress and Ongoing Concerns. Annu Rev Immunol. 2020. PMID 32340580 · DOI
- Komi DEA, Redegeld FA. Role of Mast Cells in Shaping the Tumor Microenvironment. Clin Rev Allergy Immunol. 2020. PMID 31256327 · DOI · PMC7244463
- Elieh Ali Komi D, Wöhrl S, Bielory L. Mast Cell Biology at Molecular Level: a Comprehensive Review. Clin Rev Allergy Immunol. 2020. PMID 31828527 · DOI
- Gupta K, Harvima IT. Mast cell-neural interactions contribute to pain and itch. Immunol Rev. 2018. PMID 29431216 · DOI · PMC5812374
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.