Alpha-tryptase as a risk-modifying factor for mast cell–mediated reactions
Open accessAbstract
Purpose of review To provide an overview on the current understanding of genetic variability in human tryptases and summarize the literature demonstrating the differential impact of mature tryptases on mast cell-mediated reactions and associated clinical phenotypes.Recent findings It is becoming increasingly recognized that tryptase gene composition, and in particular the common genetic trait hereditary alpha-tryptasemia (HαT), impacts clinical allergy. HαT has consistently been associated with clonal mast cell disorders (MCD) and has also been associated with more frequent anaphylaxis among these patients, and patients in whom no allergic trigger can be found, specifically idiopathic anaphylaxis. Additionally, more severe anaphylaxis among Hymenoptera venom allergy patients has been linked to HαT in both retrospective and prospective studies. An increased relative number of α-tryptase-encoding gene copies, even in the absence of HαT, has also been associated with systemic mastocytosis and has been shown to positively correlate with the severity of mast cell-mediated reactions to vibration and food. These findings may be due to increased generation of α/β-tryptase heterotetramers and differences in their enzymatic activity relative to β-tryptase homotetramers. HαT is a naturally occurring overexpression model of α-tryptase in humans. Increased relative α-tryptase expression modifies immediate hypersensitivity symptoms and is associated with more frequent and severe mast cell-mediated reactions, ostensibly due to increased α/β-tryptase heterotetramer production.
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In individuals with HαT, α/β-tryptase heterotetramers increase vascular permeability by cleaving and activating PAR2 on endothelial cells, resulting in increased vascular leakage.
“Recent studies have shown that in individuals with HαT, these heterotetramers increase vascular permeability by cleaving and activating protease-activated receptor-2 (PAR2) on endothelial cells, resulting in increased vascular leakage (14, 15).”
From Defining “Normal” basal serum tryptase levels: a context-dependent approach to improve diagnostics in systemic mastocytosis (2025) · cites this paper as [15]
The “Unique Activity of α/β-Tryptase Heterotetramers” section reports PAR2-dependent acute leakage in human endothelial cells exposed to the heterotetramers, but specifies that this was an in vitro finding. It says in vivo studies are needed, so it does not establish increased vascular leakage through this mechanism in individuals with HαT. Page numbers were not provided in our copy. (LLM, conf=0.88)
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Konnikova, L., Robinson, T. O., Owings, A. H., Shirley, J. F., Davis, E. M., Tang, Y., Wall, S. M., Li, J., Hasan, M., Gharaibeh, R. Z., et al. (2021) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2021.04.004 · Cited by 30 · see citing works
Self-citationThe Utility of Serum Tryptase as a Marker in Chronic Spontaneous Urticaria
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Disease spectrum in patients with elevated serum tryptase levels
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Self-citationSrivastava, S., Huissoon, A. P., Barrett, V., Hackett, S. J., Dorrian, S., Cooke, M. W., & Krishna, M. T. (2014) · Journal of Clinical Pathology · doi:10.1136/jclinpath-2013-202005 · Cited by 15 · see citing works
Farioli, L., Losappio, L. M., Schroeder, J. W., Preziosi, D., Scibilia, G., Caron, L., Nichelatti, M., & Pastorello, E. A. (2019) · Journal of Investigational Allergology and Clinical Immunology · doi:10.18176/jiaci.0363 · Cited by 15 · see citing works
Lyons, J. J., Chovanec, J. F., O'Connell, M. P., Liu, Y., Šelb, J., Zanotti, R., Bai, Y., Kim, J., Le, Q. T., DiMaggio, T., et al. (2020) · DiRROS repository (University of Maribor) · Cited by 13 · see citing works
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Flagged first, then by citations
Research works printed but not linked: 2
- [49]Greiner G, Sprinzl B, Gorska A, Ratzinger F, Gurbisz M, Witzeneder N, Hereditary alpha tryptasemia is a valid genetic biomarker for severe mediator-related symptoms in mastocytosis. Blood. 2020. PMC7116780 32777817
- [65]Polivka L, Madrange M, Bulai-Livideanu C, Barete S, Ballul T, Neuraz A, Pathophysiologic implications of elevated prevalence of hereditary alpha-tryptasemia in all mastocytosis subtypes. J Aller Clin Immunol. 2023. 37633651
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Hereditary Alpha-Tryptasemia (HAT) Syndrome
(2026) · Elsevier eBooks · doi:10.1016/b978-3-437-15042-5.00109-0
- Authors
- Shin, H., & Lyons, J. J.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Lyons, Jonathan J.
- Venue
- Current Allergy and Asthma Reports
- Published
- 2024-03-09
- Volume
- 24
- Issue
- 4
- Pages
- 199-209
- ISSN
- 1529-7322 (ISSN-L)
- 1534-6315
- PMC
- PMC11870015
- OpenAlex
- W4392619563
- Cited by
- 24
- References
- 88
- Citations by year
- 2026: 9 · 2025: 11 · 2024: 4
- FWCI
- 1.06
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Current Allergy and Asthma Reports (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (SI2 AI138586, R00AI138586)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Health Sciences › Medicine › Immunology and Allergy › Food Allergy and Anaphylaxis Research
- Health Sciences › Medicine › Pharmacology › Drug-Induced Adverse Reactions
- Keywords
- hereditary alpha-tryptasemia, idiopathic anaphylaxis, anaphylaxis, clonal mast cell disorders, systemic mastocytosis, hymenoptera venom allergy, genetic variation, immediate hypersensitivity, food-induced anaphylaxis
- MeSH terms
- Mast Cell Activation Syndrome, Anaphylaxis, Humans, Mast Cells, Mastocytosis, Prospective Studies, Retrospective Studies, Tryptases
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