ReviewClinical reviews in allergy & immunology
Regulation of mast cells by beta-agonists.
Review in Clinical reviews in allergy & immunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 47 citations in OpenAlex.
- The Bruton tyrosine kinase inhibitor acalabrutinib aborts ongoing acute food-induced anaphylactic reactions in humanized mice.The Journal of allergy and clinical immunology · 2025Article
- Cardiovascular manifestations in mast cell activation disease: key insights for cardiologists and angiologists.Frontiers in cardiovascular medicine · 2025Review
- Research Advances in Mast Cell Biology and Their Translation Into Novel Therapies for Anaphylaxis.The journal of allergy and clinical immunology. In practice · 2023Review
- Mast Cells in Upper and Lower Airway Diseases: Sentinels in the Front Line.International journal of molecular sciences · 2023Review
- Nonrespiratory Comorbidities in Asthma.The journal of allergy and clinical immunology. In practice · 2021Review
- Association of histamine with hypertension-induced cardiac remodeling and reduction of hypertrophy with the histamine-2-receptor antagonist famotidine compared with the beta-blocker metoprolol.Hypertension research : official journal of the Japanese Society of Hypertension · 2018Article
- The pathophysiology of anaphylaxis.The Journal of allergy and clinical immunology · 2017Review
- Vesicular trafficking and signaling for cytokine and chemokine secretion in mast cells.Frontiers in immunology · 2014Review
- The immunology of stroke: from mechanisms to translation.Nature medicine · 2011Review
- Vasculitis: current status and future directions.Clinical reviews in allergy & immunology · 2008Article
- Cutting edge issues in autoimmunity.Clinical reviews in allergy & immunology · 2008Article
- Whither autoimmunity: the lessons of anti-CCP and B cell depletion.Clinical reviews in allergy & immunology · 2008Article
- G protein-coupled receptors and the modification of FcepsilonRI-mediated mast cell activation.Immunology letters · 2007Review
- Dermal immunopathology: from genetics to effector mechanisms.Clinical reviews in allergy & immunology · 2007Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human lung mast cell is known to be a critical effector cell in the mediation of asthma. Activation of the mast cell by allergens and other stimuli leads to the release and generation of a wide variety of autacoids that cause bronchoconstriction, promote inflammation, and may influence airway remodeling. Therefore, the stabilization of mast cells has obvious value in the prevention of asthma. Among the drugs used to treat asthma, only beta-agonists are effective stabilizers of mast cells. Both short- and long-acting beta-agonists are effective against mast cells, but there are differences between agonists regarding the extent of inhibitory activity attained. Consequently, the type of beta-agonist prescribed influences the degree of mast cell stabilization possible. Despite the potential value of attenuating mast cell activity with beta-agonists, this benefit may diminish with time because of the development of tolerance. Both short- and long-acting beta-agonists can induce tolerance to mast cell stabilization, and generally, higher efficacy agonists tend to induce greater levels of tolerance; however, weaker agonists induce greater levels of tolerance than might be expected. Tolerance to the mast-cell-stabilizing effects of beta- agonists may be an issue clinically, because this occurs more readily than tolerance to smooth muscle relaxation. This could lead to a situation in which beta-agonists fail to prevent the release of mediators from mast cells but can still effectively relax airway smooth muscle. The continued ability to bronchodilate could mask the unfavorable consequences of unchecked mediator release from mast cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.