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Journal articles on the topic 'Mast cell activation disorders'

Author: Grafiati

Published: 4 June 2025

Last updated: 1 August 2025

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1

Giannetti, Arianna, Emanuele Filice, Carlo Caffarelli, Giampaolo Ricci, and Andrea Pession. "Mast Cell Activation Disorders." Medicina 57, no. 2 (2021): 124. http://dx.doi.org/10.3390/medicina57020124.

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Background and Objectives: Mast cell disorders comprise a wide spectrum of syndromes caused by mast cells’ degranulation with acute or chronic clinical manifestations. Materials and Methods: In this review article we reviewed the latest findings in scientific papers about mast cell disorders with a particular focus on mast cell activation syndrome and mastocytosis in pediatric age. Results: Patients with mast cell activation syndrome have a normal number of mast cells that are hyperreactive upon stimulation of various triggers. We tried to emphasize the diagnostic criteria, differential diagno

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Akin, Cem. "Mast Cell Activation Disorders." Journal of Allergy and Clinical Immunology: In Practice 2, no. 3 (2014): 252–57. http://dx.doi.org/10.1016/j.jaip.2014.03.007.

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Jackson, Clayton Webster, Cristina Marie Pratt, Chase Preston Rupprecht, Debendra Pattanaik, and Guha Krishnaswamy. "Mastocytosis and Mast Cell Activation Disorders: Clearing the Air." International Journal of Molecular Sciences 22, no. 20 (2021): 11270. http://dx.doi.org/10.3390/ijms222011270.

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Mast cells are derived from hematopoietic stem cell precursors and are essential to the genesis and manifestations of the allergic response. Activation of these cells by allergens leads to degranulation and elaboration of inflammatory mediators, responsible for regulating the acute dramatic inflammatory response seen. Mast cells have also been incriminated in such diverse disorders as malignancy, arthritis, coronary artery disease, and osteoporosis. There has been a recent explosion in our understanding of the mast cell and the associated clinical conditions that affect this cell type. Some ma

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Petra, Anastasia I., Smaro Panagiotidou, Julia M. Stewart, Pio Conti, and Theoharis C. Theoharides. "Spectrum of mast cell activation disorders." Expert Review of Clinical Immunology 10, no. 6 (2014): 729–39. http://dx.doi.org/10.1586/1744666x.2014.906302.

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Picard, Matthieu, Pedro Giavina-Bianchi, Veronica Mezzano, and Mariana Castells. "Expanding Spectrum of Mast Cell Activation Disorders: Monoclonal and Idiopathic Mast Cell Activation Syndromes." Clinical Therapeutics 35, no. 5 (2013): 548–62. http://dx.doi.org/10.1016/j.clinthera.2013.04.001.

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6

Hsieh, Fred H. "Gastrointestinal Involvement in Mast Cell Activation Disorders." Immunology and Allergy Clinics of North America 38, no. 3 (2018): 429–41. http://dx.doi.org/10.1016/j.iac.2018.04.008.

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7

Broesby-Olsen, Sigurd, Melody Carter, Henrik Fomsgaard Kjaer, et al. "Pediatric Expression of Mast Cell Activation Disorders." Immunology and Allergy Clinics of North America 38, no. 3 (2018): 365–77. http://dx.doi.org/10.1016/j.iac.2018.04.009.

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Akin, Cem. "How to evaluate the patient with a suspected mast cell disorder and how/when to manage symptoms." Hematology 2022, no. 1 (2022): 55–63. http://dx.doi.org/10.1182/hematology.2022000366.

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Abstract Mast cell disorders include mastocytosis and mast cell activation syndromes. Mastocytosis is a rare clonal disorder of the mast cell, driven by KIT D816V mutation in most cases. Mastocytosis is diagnosed and classified according to World Health Organization criteria. Mast cell activation syndromes encompass a diverse group of disorders and may have clonal or nonclonal etiologies. Hematologists may be consulted to assist in the diagnostic workup and/or management of mast cell disorders. A consult to the hematologist for mast cell disorders may provoke anxiety due to the rare nature of

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Zhang, Simin, and Jonathan A. Bernstein. "Mast cell activation syndrome: Myths and realities." Allergy and Asthma Proceedings 42, no. 3 (2021): 198–204. http://dx.doi.org/10.2500/aap.2021.42.210012.

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Background: Mast cells (MCs) have been implicated in a spectrum of allergic, immunologic, and infectious inflammatory conditions that involve different organ systems. MC activation can occur through several different surface receptors other than the well known IgE mediated pathway. Methods: We use two representative case reports from our practice to summarize what is currently known about MCAS disorders (reality) so that the clinician can more easily differentiate these conditions from other complex unexplained conditions that are being associated with MC activation (myth). Results: Many compl

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Friesen, Hunter, Meenal Singh, Vivekanand Singh, Jennifer V. Schurman, and Craig A. Friesen. "A Survey of Methodologies for Assessing Mast Cell Density and Activation in Patients with Functional Abdominal Pain Disorders." Gastrointestinal Disorders 3, no. 4 (2021): 142–55. http://dx.doi.org/10.3390/gidisord3040016.

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The aim was to assess methods utilized in assessing mast cell involvement in functional abdominal pain disorders (FAPDs), specifically to describe variability in methods utilized to assess both mast cell density and activation and determine if a consensus exists. After a literature search identified 70 manuscripts assessing mast cell density, data were extracted including FAPD diagnosis, site of biopsy, selection of microscopic fields analyzed, selection of mucosal region analyzed, method of mast cell identification, method to assess mast cell density, and if performed, method to assess mast c

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Weinstock, Leonard B., Renee M. Nelson, and Svetlana Blitshteyn. "Neuropsychiatric Manifestations of Mast Cell Activation Syndrome and Response to Mast-Cell-Directed Treatment: A Case Series." Journal of Personalized Medicine 13, no. 11 (2023): 1562. http://dx.doi.org/10.3390/jpm13111562.

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Mast cell activation syndrome (MCAS) is an immune disease with an estimated prevalence of 17%. Mast cell chemical mediators lead to heterogeneous multisystemic inflammatory and allergic manifestations. This syndrome is associated with various neurologic and psychiatric disorders, including headache, dysautonomia, depression, generalized anxiety disorder, and many others. Although MCAS is common, it is rarely recognized, and thus, patients can suffer for decades. The syndrome is caused by aberrant mast cell reactivity due to the mutation of the controller gene. A case series is presented herein

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Gülen, Theo. "A Puzzling Mast Cell Trilogy: Anaphylaxis, MCAS, and Mastocytosis." Diagnostics 13, no. 21 (2023): 3307. http://dx.doi.org/10.3390/diagnostics13213307.

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Our knowledge of biology and mast cell (MC) function, as well as disorders associated with the pathologic activation of MCs, has evolved over the last few decades. Anaphylaxis, mast cell activation syndrome (MCAS), and mastocytosis are interrelated yet distinct conditions within the spectrum of mast cell activation disorders. Nevertheless, all three conditions can co-exist in one and the same patient, as pathologic MC activation is the key finding in all three. When mediator release is excessive and involves multiple systems, anaphylaxis and MCAS may occur. Furthermore, mastocytosis is a clona

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13

Shibao, Cyndya, Carmen Arzubiaga, L. Jackson Roberts, et al. "Hyperadrenergic Postural Tachycardia Syndrome in Mast Cell Activation Disorders." Hypertension 45, no. 3 (2005): 385–90. http://dx.doi.org/10.1161/01.hyp.0000158259.68614.40.

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Lepelley, Marion, Charles Khouri, Pauline Pralong, et al. "Which opioids in case of mast cell activation disorders?" Journal of Allergy and Clinical Immunology: In Practice 7, no. 4 (2019): 1317–18. http://dx.doi.org/10.1016/j.jaip.2018.08.011.

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Lyons, David O., and Nicholas A. Pullen. "Beyond IgE: Alternative Mast Cell Activation Across Different Disease States." International Journal of Molecular Sciences 21, no. 4 (2020): 1498. http://dx.doi.org/10.3390/ijms21041498.

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Mast cells are often regarded through the lens of IgE-dependent reactions as a cell specialized only for anti-parasitic and type I hypersensitive responses. However, recently many researchers have begun to appreciate the expansive repertoire of stimuli that mast cells can respond to. After the characterization of the interleukin (IL)-33/suppression of tumorigenicity 2 (ST2) axis of mast cell activation—a pathway that is independent of the adaptive immune system—researchers are revisiting other stimuli to induce mast cell activation and/or subsequent degranulation independent of IgE. This disco

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Parente, Roberta, Valentina Giudice, Chiara Cardamone, Bianca Serio, Carmine Selleri, and Massimo Triggiani. "Secretory and Membrane-Associated Biomarkers of Mast Cell Activation and Proliferation." International Journal of Molecular Sciences 24, no. 8 (2023): 7071. http://dx.doi.org/10.3390/ijms24087071.

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Mast cells (MCs) are immune cells distributed in many organs and tissues and involved in the pathogenesis of allergic and inflammatory diseases as a major source of pro-inflammatory and vasoactive mediators. MC-related disorders are heterogeneous conditions characterized by the proliferation of MC within tissues and/or MC hyper-reactivity that leads to the uncontrolled release of mediators. MC disorders include mastocytosis, a clonal disease characterized by tissue MC proliferation, and MC activation syndromes that can be primary (clonal), secondary (related to allergic disorders), or idiopath

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Weiler, Catherine R., K. Frank Austen, Cem Akin, et al. "AAAAI Mast Cell Disorders Committee Work Group Report: Mast cell activation syndrome (MCAS) diagnosis and management." Journal of Allergy and Clinical Immunology 144, no. 4 (2019): 883–96. http://dx.doi.org/10.1016/j.jaci.2019.08.023.

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Wilder-Smith, Clive H., Asbjørn M. Drewes, Andrea Materna, and Søren S. Olesen. "Symptoms of mast cell activation syndrome in functional gastrointestinal disorders." Scandinavian Journal of Gastroenterology 54, no. 11 (2019): 1322–25. http://dx.doi.org/10.1080/00365521.2019.1686059.

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Ndaw, Victor, Patrick Paez, Marcela Taruselli, and John Ryan. "TGFb inhibits IL-33-mediated mast cell activation (INC6P.316)." Journal of Immunology 194, no. 1_Supplement (2015): 192.18. http://dx.doi.org/10.4049/jimmunol.194.supp.192.18.

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Abstract TGFβ is involved in many pathological considtions, including autoimmune disorders, cancer, and cardiovascular and allergic diseases. We have previously found that TGFβ can suppress IgE-mediated mast cell activation. IL-33 is a recently discovered member of the IL-1 family that plays a critical role in mast cell activation and enhances IgE-mediated activation. In this study, we investigated the effects of TGFβ on IL-33-mediated mast cell activation. Bone marrow-derived mast cells cultured in TGFβ -1, -2, or -3 showed reduced IL-33-mediated production of TNF, IL-6, IL-13 and MCP-1, in a

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Khalid, Muhammad Bilal, and Phil Lieberman. "Mast cell disorders and idiopathic anaphylaxis: Evaluation and management." Allergy and Asthma Proceedings 41, no. 2 (2020): 90–98. http://dx.doi.org/10.2500/aap.2020.41.190023.

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Background: Our understanding of mast cell activation disorders continues to grow, and our management of these syndromes is improving with this increase in knowledge. Despite these advances, there remain some areas of confusion. Conclusion: In this article, we discussed these areas and offered thoughts about establishing the diagnosis and management.

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Beyens, Michiel, Alessandro Toscano, Didier Ebo, Theo Gülen, and Vito Sabato. "Diagnostic Significance of Tryptase for Suspected Mast Cell Disorders." Diagnostics 13, no. 24 (2023): 3662. http://dx.doi.org/10.3390/diagnostics13243662.

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Tryptase has proven to be a very useful and specific marker to demonstrate mast cell activation and degranulation when an acute (i.e., within 4 h after the event) and baseline value (i.e., at least 24 h after the event) are compared and meet the consensus formula (i.e., an increase of 20% + 2). The upper limit of normal determined by the manufacturer is 11.4 ng/mL; however, this boundary has been the subject of debate. According to ECNM and AIM experts, the normal range of baseline tryptase should be 1 to 15 ng/mL. A genetic trait, hereditary alpha tryptasemia, characterized by an increased al

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Álvarez-Twose, Iván, David González de Olano, Laura Sánchez-Muñoz, et al. "Clinical, biological, and molecular characteristics of clonal mast cell disorders presenting with systemic mast cell activation symptoms." Journal of Allergy and Clinical Immunology 125, no. 6 (2010): 1269–78. http://dx.doi.org/10.1016/j.jaci.2010.02.019.

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23

Theoharides, Theoharis C., Irene Tsilioni, and Huali Ren. "Recent advances in our understanding of mast cell activation – or should it be mast cell mediator disorders?" Expert Review of Clinical Immunology 15, no. 6 (2019): 639–56. http://dx.doi.org/10.1080/1744666x.2019.1596800.

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24

Lin, Wenlong, Fasheng Su, Rahul Gautam, Ning Wang, Yuanyuan Zhang та Xiaojian Wang. "Raf kinase inhibitor protein negatively regulates FcεRI-mediated mast cell activation and allergic response". Proceedings of the National Academy of Sciences 115, № 42 (2018): E9859—E9868. http://dx.doi.org/10.1073/pnas.1805474115.

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The signaling cascades triggered by the cross-linkage of immunoglobulin E (IgE) with its high-affinity receptor (FcεRI) on mast cells contribute to multiple allergic disorders, such as asthma, rhinitis, and atopic dermatitis. Restraint of intracellular signals for mast cell activation is essential to restore homeostasis. In this study, we found that Raf kinase inhibitor protein (RKIP) negatively regulated mast cell activation. RKIP-deficient mast cells showed greater IgE−FcεRI-mediated activation than wild-type mast cells. Consistently, RKIP deficiency in mast cells rendered mice more sensitiv

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Roizen, Gigia, Corey Peruffo, and Anne L. Maitland. "Mast Cell Activation Disorders In The Setting Of Idiopathic CD4 Lymphopenia." Journal of Allergy and Clinical Immunology 141, no. 2 (2018): AB23. http://dx.doi.org/10.1016/j.jaci.2017.12.072.

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26

Ishimaru, Kayoko, Shotaro Nakajima, Guannan Yu, Yuki Nakamura, and Atsuhito Nakao. "The Putatively Specific Synthetic REV-ERB Agonist SR9009 Inhibits IgE- and IL-33-Mediated Mast Cell Activation Independently of the Circadian Clock." International Journal of Molecular Sciences 20, no. 24 (2019): 6320. http://dx.doi.org/10.3390/ijms20246320.

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The cell-autonomous circadian clock regulates IgE- and IL-33-mediated mast cell activation, both of which are key events in the development of allergic diseases. Accordingly, clock modifiers could be used to treat allergic diseases, as well as many other circadian-related diseases, such as sleep and metabolic disorders. The nuclear receptors REV-ERB-α and -β (REV-ERBs) are crucial components of the circadian clockwork. Efforts to pharmacologically target REV-ERBs using putatively specific synthetic agonists, particularly SR9009, have yielded beneficial effects on sleep and metabolism. Here, we

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Afrin, Lawrence B., Tania T. Dempsey, and Leonard B. Weinstock. "Post-HPV-Vaccination Mast Cell Activation Syndrome: Possible Vaccine-Triggered Escalation of Undiagnosed Pre-Existing Mast Cell Disease?" Vaccines 10, no. 1 (2022): 127. http://dx.doi.org/10.3390/vaccines10010127.

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For nearly a decade, case reports and series have emerged regarding dysautonomias—particularly postural orthostatic tachycardia syndrome (POTS)—presenting soon after vaccination against human papilloma virus (HPV). We too have observed a number of such cases (all following vaccination with the Gardasil product), and have found several to have detectable mast cell activation syndrome (MCAS) as well as histories suggesting that MCAS was likely present long before vaccination. We detail 11 such cases here, posing a hypothesis that HPV vaccination (at least with the Gardasil product) may have trig

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Giannetti, Matthew P., Emily Weller, Iván Alvarez-Twose, et al. "COVID-19 infection in patients with mast cell disorders including mastocytosis does not impact mast cell activation symptoms." Journal of Allergy and Clinical Immunology: In Practice 9, no. 5 (2021): 2083–86. http://dx.doi.org/10.1016/j.jaip.2021.02.023.

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Leoni, Cristina, Sara Montagner, Andrea Rinaldi, et al. "Dnmt3arestrains mast cell inflammatory responses." Proceedings of the National Academy of Sciences 114, no. 8 (2017): E1490—E1499. http://dx.doi.org/10.1073/pnas.1616420114.

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DNA methylation and specifically the DNA methyltransferase enzyme DNMT3A are involved in the pathogenesis of a variety of hematological diseases and in regulating the function of immune cells. Although altered DNA methylation patterns and mutations inDNMT3Acorrelate with mast cell proliferative disorders in humans, the role of DNA methylation in mast cell biology is not understood. By using mast cells lackingDnmt3a, we found that this enzyme is involved in restraining mast cell responses to acute and chronic stimuli, both in vitro and in vivo. The exacerbated mast cell responses observed in th

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Muñoz-González, Javier Ignacio, Andres C. Garcia-Montero, Alberto Orfao, and Iván Alvarez-Twose. "Pathogenic and diagnostic relevance of KIT in primary mast cell activation disorders." Annals of allergy, asthma, & immunology 127, no. 4 (2021): 1–8. https://doi.org/10.1016/j.anai.2021.07.014.

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Mast cell (MC) activation (MCA) defines the mechanism by which certain patients have symptomsowing to the effect of a wide range of mediators released from MCs upon their activation, when triggered by different stimuli. When these symptoms are severe and recurrent, the diagnosis of MCA syndrome (MCAS) might be considered. Here, we review the relevant aspects related to the pathogenesis of MCAS, with special emphasis on the prevalence and diagnostic relevance of KIT mutations.

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Romantowski, Jan, Aleksandra Górska, Marek Niedoszytko, et al. "A Challenge for Allergologist: Application of Allergy Diagnostic Methods in Mast Cell Disorders." International Journal of Molecular Sciences 22, no. 3 (2021): 1454. http://dx.doi.org/10.3390/ijms22031454.

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Primary and secondary mast cell activation syndromes (MCAS) can occur in patients with mastocytosis. During the past few years our knowledge about the pathogenesis and disease-triggering mechanisms in MCAS and mastocytosis have increased substantially. Whereas mastocytosis is characterized by an accumulation of neoplastic (clonal) mast cells (MC) in various organ systems, MCAS is defined by a massive and systemic activation of these cells. Mast cells are crucial effector cells in allergic diseases, thus their elevated number and activation can cause severe anaphylactic reactions and MCAS in pa

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Edelson, Brian T., Thomas P. Stricker, Zhengzhi Li, et al. "Novel collectin/C1q receptor mediates mast cell activation and innate immunity." Blood 107, no. 1 (2006): 143–50. http://dx.doi.org/10.1182/blood-2005-06-2218.

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Abstract Mast cells play a critical role in innate immunity, allergy, and autoimmune diseases. The receptor/ligand interactions that mediate mast cell activation are poorly defined. The α2β1 integrin, a receptor for collagens, laminins, decorin, E-cadherin, matrix metalloproteinase-1 (MMP-1), endorepellin, and several viruses, has been implicated in normal developmental, inflammatory, and oncogenic processes. We recently reported that α2 integrin subunit–deficient mice exhibited markedly diminished neutrophil and IL-6 responses during Listeria monocytogenes–and zymosan-induced peritonitis. Per

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Molina, Irina Miralda, Nyssa B. Samanas, Albert J. Seo, et al. "Dedicator of cytokinesis 8 (DOCK8) is a negative regulator of skin mast cell function." Journal of Immunology 210, no. 1_Supplement (2023): 151.04. http://dx.doi.org/10.4049/jimmunol.210.supp.151.04.

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Abstract Dysregulated expansion and/or activation of mast cells have detrimental consequences in allergic disease. In humans, homozygous or compound heterozygous deletions of DOCK8 cause a combined immunodeficiency characterized by allergic disorders. Based on this evidence, we hypothesized that DOCK8 may be a negative regulator of mast cell function. To address this hypothesis, we used mice with a loss-of-function mutation in Dock8 (primuris, Dock8 pri/primice) and conditional mice in which DOCK8 is ablated in connective tissue mast cells (Mcpt5-Cre +; Dock8 fl/flmice). Dock8 pri/primice exhi

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Vera, Mariano Ezequiel, María Laura Mariani, Cristina Aguilera, and Alicia Beatriz Penissi. "Effect of a Cytoprotective Dose of Dehydroleucodine, Xanthatin, and 3-Benzyloxymethyl-5H-furan-2-one on Gastric Mucosal Lesions Induced by Mast Cell Activation." International Journal of Molecular Sciences 22, no. 11 (2021): 5983. http://dx.doi.org/10.3390/ijms22115983.

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The aim of this study was to determine whether the lactones dehydroleucodine, xanthatin and 3-benzyloxymethyl-5H-furan-2-one, would be effective in an animal model of gastric ulcer induced by mast cell activation. Rats were divided into ten groups. Treatments were repeated for four days. The degree of gastric erosion was assessed with a scoring system and histological preparations. Gastric mast cell morphology was analyzed by histological procedures. Serum serotonin levels were determined as markers of mast cell activation. Statistical analyses were done using ANOVA and Tukey–Kramer test. We d

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Afrin, Lawrence B. "Burning mouth syndrome and mast cell activation disorder." Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 111, no. 4 (2011): 465–72. http://dx.doi.org/10.1016/j.tripleo.2010.11.030.

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Roberts, L. Jackson. "Carcinoid Syndrome and Disorders of Systemic Mast-Cell Activation Including Systemic Mastocytosis." Endocrinology and Metabolism Clinics of North America 17, no. 2 (1988): 415–36. http://dx.doi.org/10.1016/s0889-8529(18)30427-4.

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Weinstock, Leonard B., Lawrence B. Afrin, Angela M. Reiersen, et al. "Prevalence and treatment response of neuropsychiatric disorders in mast cell activation syndrome." Brain, Behavior, & Immunity - Health 48 (October 2025): 101048. https://doi.org/10.1016/j.bbih.2025.101048.

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Afrin, Lawrence B. "Mast cell activation disorder masquerading as pure red cell aplasia." International Journal of Hematology 91, no. 5 (2010): 907–8. http://dx.doi.org/10.1007/s12185-010-0605-x.

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Jeong, Hyun-Ja, Ho-Jeong Na, Seung-Heon Hong, and Hyung-Min Kim. "Inhibition of the Stem Cell Factor-Induced Migration of Mast Cells by Dexamethasone." Endocrinology 144, no. 9 (2003): 4080–86. http://dx.doi.org/10.1210/en.2003-0115.

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Abstract Mast cell accumulation can be causally related to several allergic inflammations. Previous work has demonstrated that glucocorticoids decreased tissue mast cell number, and stem cell factor (SCF)-induced migration of mast cells required p38 MAPK activation. In the present study we investigated the effects of dexamethasone on SCF-induced migration of rat peritoneal mast cells (RPMCs). SCF significantly induced the migration of RPMCs at 4 h. Dexamethasone dose-dependently inhibited SCF-induced migration of RPMCs (∼90.1% at 100 nm; P &lt; 0.05). The MAPK p38 inhibitor SB203580 (20 μm

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Gordon, J. R., and S. J. Galli. "Promotion of mouse fibroblast collagen gene expression by mast cells stimulated via the Fc epsilon RI. Role for mast cell-derived transforming growth factor beta and tumor necrosis factor alpha." Journal of Experimental Medicine 180, no. 6 (1994): 2027–37. http://dx.doi.org/10.1084/jem.180.6.2027.

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Chronic allergic diseases and other disorders associated with mast cell activation can also be associated with tissue fibrosis, but a direct link between mast cell mediator release and fibroblast collagen gene expression has not been established. Using in situ hybridization, we show that the elicitation of an IgE-dependent passive cutaneous anaphylaxis (PCA) reaction in mice results in a transient, but marked augmentation of steady state levels of type alpha-1 (I) collagen mRNA in the dermis. While peak levels of collagen mRNA expression in the skin are observed 16-24 h after mast cell activat

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Shin, Jinwook, Hongjie Pan, and Xiao-Ping Zhong. "Regulation of mast cell survival and function by tuberous sclerosis complex 1." Blood 119, no. 14 (2012): 3306–14. http://dx.doi.org/10.1182/blood-2011-05-353342.

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Abstract Mast cells play critical roles in allergic disorders and asthma. The importance of tuberous sclerosis complex 1/2-mammalian target of rapamycin (TSC1/2-mTOR) signaling in mast cells is unknown. Here, we report that TSC1 is a critical regulator for mTOR signaling in mast cells downstream of FcεRI and c-Kit, and differentially controls mast cell degranulation and cytokine production. TSC1-deficiency results in impaired mast cell degranulation, but enhanced cytokine production in vitro and in vivo after FcεRI engagement. Furthermore, TSC1 is critical for mast cell survival through multip

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Bandara, Geethani, Yun Bai, Eunice Ching Chan, et al. "Targeting the KIT Activating Switch Control Pocket: A Novel Mechanism to Inhibit Mast Cell Activation and KIT D816V Neoplastic Mast Cell Proliferation." Blood 118, no. 21 (2011): 1740. http://dx.doi.org/10.1182/blood.v118.21.1740.1740.

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Abstract Abstract 1740 KIT is a receptor protein tyrosine kinase which undergoes dimerization, autophysophyralation, and activation upon binding of its ligand, stem cell factor (SCF). Such activation is critical for the growth, differentiation and survival of mast cells. By enhancing Fcƒ'RI-mediated degranulation and inducing chemotaxis, KIT also contributes to mast cell functional responses. Targeting KIT is thus an attractive approach for the management of proliferative mast cell disorders. Activating mutations in the KIT tyrosine kinase domain, most notably KIT D816V, are commonly observed

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Valent, Peter, Cem Akin, Michel Arock, et al. "Definitions, Criteria and Global Classification of Mast Cell Disorders with Special Reference to Mast Cell Activation Syndromes: A Consensus Proposal." International Archives of Allergy and Immunology 157, no. 3 (2012): 215–25. http://dx.doi.org/10.1159/000328760.

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Aye, Cho Cho, and Santa Ono. "Chemokine receptor signaling in mast cells (89.27)." Journal of Immunology 178, no. 1_Supplement (2007): S154. http://dx.doi.org/10.4049/jimmunol.178.supp.89.27.

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Abstract Mast cells play an important role in IgE-associated allergic disorders and immune response to parasites. In a former study, we demonstrated that chemokine CCL3 (MIP-1α) acted as a co-stimulator for FcεRI-mediated activation on mast cells. To advance our understanding on this finding, we studied gene profiles in Rat Basophilic Leukaemia mast cells after co-activation of CCR1 (a receptor of CCL3) and FcεRI using the Affymetrix GeneChip Arrays. Emp1 (Epithelial Membrane protein 1), RT1-S3 (non-classical type 1 MHC gene), and Slc35e4 (solute carrier family 35, member E4) were found to be

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B. Weinstock, Leonard, Andrew W. Campbell, Luke Curtis, and Jordan Gutovich. "Mycotoxin-Triggered Attacks of Nausea, Vomiting, and Abdominal Pain and Episodes of Pseudo-Obstruction." Universal Library of Medical and Health Sciences 02, no. 01 (2024): 59–69. http://dx.doi.org/10.70315/uloap.ulmhs.2024.0201008.

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Determining the etiology of episodic abdominal pain, nausea and vomiting with and without pseudo-obstruction and implementing effective treatment can be challenging. Mycotoxins activate mast cells which rapidly degranulate releasing pro-inflammatory cytokines. Mast cells commonly reside in the gastrointestinal mucosa and adjacent to nerves. Aberrant mast cells with loss of control due to genetic abnormalities are present in mast cell activation syndrome, a common, yet often unrecognized multisystemic disorder. Mold exposure with consequent toxicity by its mycotoxins can present with complex mu

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Ndaw, Victor S., Elizabeth Motunrayo Kolawole, Daniel Abebayehu та ін. "TGFβ inhibits IL-33-mediated mast cell activation in vitro and in vivo". Journal of Immunology 196, № 1_Supplement (2016): 51.16. http://dx.doi.org/10.4049/jimmunol.196.supp.51.16.

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Abstract TGFβ is involved in many pathological conditions, including autoimmune disorders, cancer, and cardiovascular and allergic diseases. We have previously found that TGFβ suppresses IgE-mediated mast cell activation in human and mouse mast cells in vitro. IL-33 is a recently discovered member of the IL-1 family that functions as an “alarmin” stimulating mast cell responses and enhancing IgE-mediated activation. How TGFβ affects IL-33 signaling is now known. We find that mouse bone marrow-derived mast cells cultured in TGFβ -1, -2, or -3 showed reduced IL-33-mediated production of TNF, IL-

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Wong, Sammi, Sara Hasan, Christina Parducci, and Bernadette Ann Riley. "The gastrointestinal effects amongst Ehlers-Danlos syndrome, mast cell activation syndrome and postural orthostatic tachycardia syndrome." AIMS Allergy and Immunology 6, no. 2 (2022): 19–24. http://dx.doi.org/10.3934/allergy.2022004.

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<abstract> <p>Ehlers-Danlos syndrome (EDS), mast cell activation syndrome, and postural orthostatic tachycardia syndrome are a triad of comorbid conditions that can occur simultaneously in many patients. Specifically, Ehlers-Danlos syndrome is a group of inherited connective tissue disorders that weakens the connective tissue and causes easy bruising. Mast cell activation syndrome (MCAS) is a condition in the connective tissue of vascularized organs that causes recurrent episodes of anaphylactic symptoms. The irregular activation of mast cells may contribute to immunological manife

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Nguyen, Anh P., and Suzanne S. Teuber. "Mast cell activation disorder masquerading as a nervous breakdown." Case Reports in Internal Medicine 4, no. 3 (2017): 51. http://dx.doi.org/10.5430/crim.v4n3p51.

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While mast cells have been implicated in human disease since the early 1900s, mast cell activation syndrome (MCAS) was only recently discovered and recognized as a disorder caused by aberrant release of mast cell mediator enzymes. These mediators trigger a wide variety of symptoms ranging from headache, pruritis and gastrointestinal discomfort to life-threatening anaphylaxis. MCAS is frequently unrecognized and misdiagnosed because symptoms associated with MCAS are often present in other medical conditions and are highly variable among patients. We describe a case of a 62-year-old male who pre

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Perales Chordá, Carolina, Sandra Fabregat Nebot, Pedro Moral Moral, Isidro Jarque Ramos, and Dolores Hernández Fernandez de Rojas. "Syncope as a manifestation of mast cell activation disorder." Annals of Allergy, Asthma & Immunology 114, no. 2 (2015): 153–54. http://dx.doi.org/10.1016/j.anai.2014.11.019.

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LeMon, Janelle, Nidia Maradiaga, and Adam James Moeser. "Early life adversity programs a hyperactive mast cell phenotype and induces long-lasting changes in the mast cell transcriptome." Journal of Immunology 208, no. 1_Supplement (2022): 49.22. http://dx.doi.org/10.4049/jimmunol.208.supp.49.22.

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Abstract Early life adversity (ELA) induces long-lasting chronic low-grade immune activation and increases the risk for inflammatory and metabolic disorders later in life. Our previous studies demonstrated that mast cells (MCs) which are well-established orchestrators of immune responses and as effector cells of the stress response exhibit heightened reactivity to later life stressors. Here, we used a murine model of ELA (neonatal maternal separation + early weaning; NMSEW) to determine the long-lasting programming effects of ELA on MC phenotype and function. Bone marrow-derived mast cells (BM

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