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Dissertations / Theses on the topic 'Mast cell activation disorders'

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Published: 4 June 2025

Last updated: 1 August 2025

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1

Endoh, Ikuko Medical Sciences Faculty of Medicine UNSW. "New mechanisms of regulation of mast cell activation." Publisher:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/42937.

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Mast cells (MCs) play a central role in inflammation by releasing mediators following activation. S100A8 and S100A9 are abundantly expressed in inflammatory sites such as asthmatic lung, sunburnt skin and atherosclerosis where MCs are involved in pathogenesis; roles of S100A8 in MC function are undetermined. The aims of this thesis were to determine effects of S100A8 on MC activation, particularly provoked by IgE and UVB. Initially, effects of UVB on MC activation were investigated as detailed functions were unclear. Cord blood-derived human mast cells (CBMCs) were treated in vitro with varyin

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2

Koranteng, Rachael Darkoa. "Effects of nitric oxide on mast cell activation." Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343761.

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3

Collmann, Emilie. "Role of phosphoindositide 3-kinases in mast cell activation /." [S.l.] : [s.n.], 2009. http://edoc.unibas.ch/diss/DissB_8779.

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4

Versani, Maheshkumar Premji. "The role of phospholipase A2 in mast cell activation." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286756.

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5

Alic, Arna. "Involvement of proteases and kinases in mast cell activation." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251972.

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6

Faber, Travis. "ADAM10: a Novel Regulator of Mast Cell Function and Activation." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/354.

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In this study we show, to our knowledge, the first description of the role ADAM10 plays on mast cells. ADAM10 is abundantly expressed on mast cells both in vitro and in vivo. Its expression is inhibited by IL-10, a suppressive cytokine. siRNA depletion of ADAM10 on bone marrow-derived mast cells (BMMC) caused decreased IL-6 production following IgE cross-linking and also impaired BMMC stem cell factor (SCF)-induced migration through collagen IV. Mast cells and T helper cells (Th cells) in the peritoneum were reduced in ADAM10 KO mice. In addition, ADAM10 KO BMMC produced significantly less of

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7

Clements, Ruth Jocelyn Muriel. "Mast cell recruitment and activation as measures of cyathostomin burden." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15853.

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Cyathostomins are potentially life threatening parasitic nematodes of adult horses and are highly prevalent worldwide. Infected animals may be asymptomatic or show clinical signs of weight loss, diarrhoea and colic. Third and fourth stage larvae spend a large proportion of their lifecycle encysted in the large intestinal wall where they cannot currently be detected ante mortem. Mast cells are commonly found at interfaces to the external environment, such as the rectum, and these cells and the proteinases they produce have been implicated in protective host immune responses against nematode inf

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8

Haaster, Charles Marie Catharine Joseph van. "Mast cell activation and mediator release implications for the cardiovascular system /." [Maastricht : Maastricht : Rijksuniversiteit Limburg] ; University Library, Maastricht University [Host], 1996. http://arno.unimaas.nl/show.cgi?fid=6684.

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9

Hallgren, Jenny. "The role of heparin in the activation of mast cell tryptase /." Uppsala : Dept. of Molecular Biosciences, Swedish Univ. of Agricultural Sciences, 2004. http://epsilon.slu.se/v179.pdf.

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10

Chernushevich, Oksana I. "THE EFFECT OF DEXAMETHASONE ON IL-33-MEDIATED MAST CELL ACTIVATION." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3772.

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Dexamethasone has been shown to inhibit IgE-mediated mast cell activation, and the present research investigated its role in suppressing IL-33-mediated mast cell activation. We have found that micromolar concentrations of Dexamethasone are capable of suppressing IL-33-mediated mast cell cytokine production, on several genetic backgrounds, and in not only bone marrow derived mast cells, but also peritoneal mast cells. Intracellular staining demonstrated that Dexamethasone significantly reduces expression of the IL-33 receptor, T1/ST2, in mast cells; however, the cytokine suppression is independ

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11

Benyon, R. C. "Studies on the purported role of lipid methylation in mast cell activation." Thesis, University of Southampton, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377417.

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12

O'Sullivan, Siobhán. "On the role of PGD₂ metabolites as markers of mast cell activation in asthma /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3243-3.

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13

Gulliksson, Magdalena. "Mast cell activation in response to osmotic and immunological stimulation with focus on release of eicosanoid mediators /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-091-6/.

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14

Geldman, Alexander. "Role of PTP-alpha in integrated c-Kit and Fc-epsilon R1 mast cell activation." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/40340.

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Mast cells (MCs) play a crucial role in the induction of allergic asthma by secreting inflammatory mediators in response to allergens. In addition to MC activation via the antigen/IgE receptor FcεR1, MC tissue recruitment and responsiveness is greatly enhanced by co-stimulation with the stem cell factor (SCF). Levels of SCF are elevated in the asthmatic lung, where it stimulates the c-Kit receptor on MCs. Sufficient signaling through c-Kit and FcεR1 requires the activation of Src family kinases, which can be regulated by protein tyrosine phosphatase alpha (PTPα). Our lab has previously demonst

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15

Ludwig, Desiree. "Measurement of mast cell and basophil activation in vitro as means for investigation of drug hypersensitivity." Thesis, University of Southampton, 2015. https://eprints.soton.ac.uk/416617/.

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Allergic drug reactions to drugs are becoming more frequent throughout the world and are among the most common and serious form of immuno-pathological process in modern clinical medicine. These reactions can lead to life-threatening anaphylaxis which can occur within minutes of receiving the drug. Symptoms provoked by the explosive release of mediators from mast cells and basophils release may include itchiness, angioedema, difficulty breathing and circulatory collapse. There are few reliable laboratory tests available to identify those with drug hypersensitivity who may be at risk of anaphyla

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16

Perng, Diahn-Warng. "The proinflammatory actions of mast cell tryptase and agonists of protease activated receptor 2 on the human airway epithelium." Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327262.

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17

Paranjape, Anuya. "MAST CELL ACTIVATION BY DIVERSE STIMULI CAN BE SUPPRESSED BY STEROID THERAPY AND TARGETING THE FYN-STAT5B CASCADE." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/5069.

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Mast cells are critical effectors of allergic disease that can be activated by numerous stimuli. We have examined mast cell control by the inflammatory cytokine, IL-33, as well as IgG. In the first study reported here, we found that the synthetic glucocorticoid, dexamethasone, potently and rapidly suppressed IL-33-induced cytokine production from murine bone marrow–derived and peritoneal mast cells, as well as human mast cells. Dexamethasone also antagonized IL-33-mediated enhancement of IgE-induced cytokine production and migration. Although dexamethasone had no effect on IL-33-induced phosph

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18

Aguilera, Rojas Matias Ignacio [Verfasser]. "Cellular crosstalk between canine fibroblasts and a mast cell tumour cell line and its significance in fibroblast activation / Matias Ignacio Aguilera Rojas." Berlin : Freie Universität Berlin, 2020. http://d-nb.info/1218530553/34.

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19

Hollins, Fay Marie. "Human airway smooth muscle promotion of mast cell survival and proliferation, and altered state of activation in asthma." Thesis, University of Leicester, 2009. http://hdl.handle.net/2381/4794.

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Asthma is a condition that is characterized by variable airflow obstruction, airway hyperresponsiveness (AHR), chronic airway inflammation and airway remodeling. There is microlocalisation of mast cells within the airway smooth muscle (ASM) bundle in asthma at a level significantly above health and other respiratory diseases. These cells are recruited and their survival promoted. However, their functional consequences have yet to be discovered. AHR in asthma is a result of increased responsiveness of the ASM to agonist and has found to increase with localized mast cell numbers. This phenomenon

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20

Akers, Ian Arthur. "The activation of lung fibroblasts by human mast cell tryptase : a role for protease activated receptor 2 (PAR 2)." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272225.

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21

Simpson, Andrew John. "Exercise induced bronchoconstriction in athletes : influence of airway dehydration on bronchial hyper-responsiveness, epithelial injury and mast cell activation." Thesis, Brunel University, 2015. http://bura.brunel.ac.uk/handle/2438/11610.

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Exercise-induced bronchoconstriction (EIB) is the most common chronic medical condition affecting elite athletes; our understanding of the condition remains however incomplete. The over-arching aim of this thesis was therefore to investigate the underlying mechanisms of EIB in athletes. More specifically, via induced and inhibited bronchoconstriction, the influence of airway dehydration on bronchial hyper-responsiveness, epithelial injury and inflammatory mediator release was investigated. The results of our first experiment suggest that mild, whole-body dehydration does not affect the severit

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22

Caslin, Heather. "Glycolytic ATP production is required for innate mast cell activation and is limited by lactic acid, which effectively reduces LPS-induced cytokine production in mast cells and in vivo." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5383.

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The metabolic pathways required for adenosine triphosphate (ATP) production within the cell are well understood, however recent publications suggest that metabolic pathways are closely linked to immune cell activation and inflammatory diseases. There has been little examination of the metabolic pathways that modulate mast cell activation and the feedback regulator lactic acid. Here we examine metabolic pathways and regulation within mast cells in the context of lipopolysaccharide (LPS) and interleukin (IL-33) activation, for which there has been little to no reported studies. First, we examine

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23

Smyth, Lucy J. C. "Activation of cells of the mast cell/basophil lineage in response to potential allergens in the absence of IgE sensitisation." Thesis, University of Sheffield, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324450.

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24

Gast, Mathias [Verfasser], Michael [Akademischer Betreuer] Huber та Bernhard [Akademischer Betreuer] Lüscher. "Mast cell activation by supra-optimal antigen concentrations - a promising condition to identify novel regulators of FcεRI signaling / Mathias Gast ; Michael Huber, Bernhard Lüscher". Aachen : Universitätsbibliothek der RWTH Aachen, 2019. http://d-nb.info/1221697536/34.

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25

Shelton, Heath W. "The Effects of Two Novel Anti-Inflammatory Compounds On Prepulse Inhibition and Neural Microglia Cell Activation in a Rodent Model of Schizophrenia." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etd/3537.

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Recent studies have shown elevated neuroinflammation in a large subset of individuals diagnosed with schizophrenia. A pro-inflammatory cytokine, tumor necrosis factor-alpha (TNFα), has been directly linked to this neuroinflammation. This study examined the effects of two TNFα modulators (PD2024 and PD340) produced by our collaborators at P2D Bioscience, Inc., to alleviate auditory sensorimotor gating deficits and reduce microglial cell activation present in the polyinosinic:polycytidylic (Poly I:C) rodent model of schizophrenia. Auditory sensorimotor gating was assessed using prepulse inhibiti

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26

Gavériaux, Claire. "Etude de l'interaction entre l'immunoglobuline e et son recepteur de forte affinite : mise au point d'un nouvel essai immunoenzymatique sur cellules, le celisa, importance de la n-glycosylation et de l'activation de la proteine kinase c dans l'expresion fonctionnelle de ce recepteur." Université Louis Pasteur (Strasbourg) (1971-2008), 1988. http://www.theses.fr/1988STR13014.

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27

Kalesnikoff, Janet. "Regulation of mast cell activation." Thesis, 2003. http://hdl.handle.net/2429/14870.

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SH2-containing inositol 5'-phosphatase (SHIP) is a 145kDa protein that becomes both tyrosine phosphorylated and associated with the adapter protein She following the stimulation of hemopoietic cells with a variety of extracellular stimuli. SHIP typically acts as a negative regulator of hemopoietic cell activation, at least in part, by hydrolyzing the phosphatidylinositol 3'-kinase (PI3K) generated second messenger phosphatidylinositol 3,4,5-trisphosphate (PIP3). To gain further insight into SHIP'S role in mast cell development and activation, we generated bone marrow-derived mast cells (BMMCs)

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28

"Chloride influx and mast cell activation." 1999. http://library.cuhk.edu.hk/record=b5889994.

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by Wan Sze Ping.<br>Thesis (M.Phil.)--Chinese University of Hong Kong, 1999.<br>Includes bibliographical references (leaves 172-185).<br>Abstracts in English and Chinese.<br>Abstract --- p.i<br>Acknowledgements --- p.v<br>Publications --- p.vi<br>Abbreviations --- p.vii<br>Chapter Chapter 1 --- Introduction --- p.1<br>Chapter 1.1. --- Historical Background --- p.2<br>Chapter 1.2. --- Origin and heterogeneity of mast cells --- p.2<br>Chapter 1.3. --- Mast cell mediators --- p.4<br>Chapter 1.3.1. --- Preformed mediators --- p.5<br>Chapter 1.3.2. --- Newly synthesised mediators --- p.6<

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29

Machyna, Martin. "Dual role of CD9 protein in mast cell activation." Master's thesis, 2009. http://www.nusl.cz/ntk/nusl-274422.

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Mast cells are well known effector cells in immune system. They have been implicated in such important processes as host defense against bacteria, toxins or parasites. However, in some cases they can develop improper reaction against harmless environmental antigens and thus causing allergies. It is therefore essential to understand signaling events that lead to activation of these cells in order to develop new treatment strategies. Newly prepared rat monoclonal antibody of IgG1 subtype raised against murine mast cells was characterized and found suitable for flow cytometry, immunoblotting and

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30

Shaik, Gouse Mohiddin. "New signaling pathways involved in mast cell activation and cell membrane repair." Doctoral thesis, 2008. http://www.nusl.cz/ntk/nusl-274190.

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RESULTS 54 RESULTS AND DISCUSSION Vacuolin-1-induced changes in mast cells morphology In pilot experiments we determined the effect of vacuolin-1 on mast cell morphology. Incubation of RBL-2H3 cells or BMMCs with 10 μM vacuolin-1 in complete culture media for 3 h resulted in appearance of numerous vacuoles in cytosolic compartment of the cells (Fig 1A-D). Size of the vacuolin-1-treated cells rose (Fig 1E and F) as reflected by mean increase in diameter of RBL-2H3 cells from 14.8 ± 0.2 μm (mean ± S.D., n = 3) to 18.8 ± 0.3 μm, and BMMCs from 14.6 ± 0.2 μm to 17.3 ± 0.2 μm. To deci

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Deng, Zhao. "Engineered nanostructures for investigation and regulation of mast cell activation." Diss., 2009. http://proquest.umi.com/pqdweb?did=1983628911&sid=1&Fmt=2&clientId=48051&RQT=309&VName=PQD.

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32

Ang, Wei Xin Gladys. "Methods and Mechanisms of Mitigating Mast Cell Activation in Anaphylaxis." Diss., 2016. http://hdl.handle.net/10161/13409.

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<p>A great number of people suffer from allergic disorders, some of which can be serious and life threatening. Unfortunately, there are limited ways to treat or prevent these maladies, in part due to our limited understanding. This dissertation addresses a novel mechanism of rapid desensitization, a procedure used to achieve temporary tolerance to allergens to prevent anaphylaxis, a severe allergic reaction involving mast cell degranulation. Specifically, we found that desensitization results in the aberrant reorganization of the actin cytoskeleton in mast cells, preventing calcium mobilizatio

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33

"The roles of Toll-like receptor 2 on human mast cell activation." 2012. http://library.cuhk.edu.hk/record=b5549654.

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肥大細胞是過敏和炎症的主要效應細胞，其激活機制包括了IgE依賴性和非IgE依賴性的激活。IgE依賴性激活是指抗原與IgE的高親和力受體FcεRI上的IgE結合，促使FcεRI受體交聯而引起變態反應。其它的肥大細胞促分泌素如神經肽P物質，能夠激活百日咳毒素（PTX）敏感性的G蛋白而介導非IgE依賴性的細胞激活。最近的研究指出，肥大細胞表達Toll樣受體家族，提示肥大細胞也積極參與固有免疫反應。本研究主要探討Toll樣受體2激動劑肽聚糖（PGN）和合成激動劑Pam3CSK4對人類肥大細胞的影響，及其對抗原和P物質引起的肥大細胞激活的調控。<br>Toll樣受體2激動劑本身不引起人類肥大細胞脫顆粒，但抑制抗原和P物質引起的肥大細胞脫顆粒。鈣動員是引起肥大細胞脫顆粒的關鍵因素。Pam3CSK4通過抑制抗原和P物質鈣動員來抑制肥大細胞脫顆粒。PGN只抑制抗原鈣動員，卻對P物質沒有影響。<br>PGN和Pam3CSK4皆刺激人類肥大細胞釋放白細胞介素8(IL-8)和腫瘤壞死因子α（TNF-α）。Pam3CSK4通過激活G₀蛋白，Erk，Ca²⁺/calcineurin/NFAT和TAK信號通路引起肥大細胞釋放IL-8。其間，Go蛋白的激活介導Erk和Ca²⁺/calcineurin/NFAT信號通路的活化。與Pam3CSK4不同，PGN通過激活JNK, Erk, PI3K和TAK信號通路引起肥

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34

LAN, LING-YEN, and 藍舲嫣. "Inhibitory effect of Ganoderma neojaponicum on RBL-2H3 mast cell activation." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/76401014856652065247.

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35

"Osteopontin differentially regulates human mast cell functions induced by FcεRI and TLR2 activation". 2015. http://repository.lib.cuhk.edu.hk/en/item/cuhk-1291886.

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Ng, Chun Wai.<br>Thesis Ph.D. Chinese University of Hong Kong 2015.<br>Includes bibliographical references (leaves 186-237).<br>Abstracts also in Chinese.<br>Title from PDF title page (viewed on 29, November, 2016).

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Stratmann, Heidi [Verfasser]. "Studies on the role of Rac in mast cell activation / vorgelegt von Heidi Stratmann." 2010. http://d-nb.info/1007691174/34.

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37

Jin, C., CP Shelburne, G. Li, et al. "Particulate allergens potentiate allergic asthma in mice through sustained IgE-mediated mast cell activation." Thesis, 2011. http://hdl.handle.net/10161/2358.

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Allergic asthma is characterized by airway hyperresponsiveness, inflammation, and a cellular infiltrate dominated by eosinophils. Numerous epidemiological studies have related the exacerbation of allergic asthma with an increase in ambient inhalable particulate matter from air pollutants. This is because inhalable particles efficiently deliver airborne allergens deep into the airways, where they can aggravate allergic asthma symptoms. However, the cellular mechanisms by which inhalable particulate allergens (pAgs) potentiate asthmatic symptoms remain unknown, in part because most in vivo and i

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St, John Ashley Lauren. "Cellular Trafficking and Activation within Lymph Nodes: Contributions to Immunity and Pathogenic or Therapeutic Implications." Diss., 2010. http://hdl.handle.net/10161/3010.

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<p>Lymph nodes are organs of efficiency. Once activated, they essentially function to optimize and accelerate the production of the adaptive immune response, which has the potential to determine survival of the host during an initial infection and protect against repeated infections, should specific and appropriate immunological memory be sufficiently induced. We now have an understanding of the fundamental structure of lymph nodes and many of the interactions that occur within them throughout this process. Yet, lymph nodes are dynamic and malleable organs and much remains to be investigated

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Rubíková, Zuzana. "Regulační mechanizmy reorganizace mikrotubulů v aktivovaných žírných buňkách." Doctoral thesis, 2017. http://www.nusl.cz/ntk/nusl-371002.

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Microtubules (MTs) are highly dynamic structures essential for the spatio-temporal intracellular organization and transport, signal propagation, cell differentiation, motility and division. To perform these roles, MTs create arrangements capable of fast and precise adaptation to various signals. MTs are under the control of many factors regulating MT nucleation, stability and dynamics. Bone marrow-derived mast cells (BMMCs) are important immune system cells, which can cause serious diseases if their functions are deregulated. Although MT reorganization during BMMC activation is well establishe

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FAVALORO, FLORES LIETTA. "Analysis of mutations in synaptic adhesion molecules involved in neurodevelopmental disorders: cell mechanisms of endoplasmic reticulum retention and unfolded protein response activation." Doctoral thesis, 2016. http://hdl.handle.net/11573/875615.

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Several forms of monogenic autism spectrum disorders are associated to mutations in the genes encoding for the postsynaptic cell adhesion molecules, Neuroligins. The autism-linked substitution of the arginine at position 451 by a cysteine (R451C) in Neuroligin3 induces local misfolding of the extracellular domain, causing partial retention in the endoplasmic reticulum. The accumulation of misfolded proteins in the endoplasmic reticulum can eventually result in stress conditions and ultimately in the activation of the unfolded protein response. We have generated a PC12 Tet-On cell system with i

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Martin, Holly René. "Mechanism of Transformation and Therapeutic Targets for Hematological Neoplasms Harboring Oncogenic KIT Mutation." Thesis, 2014. http://hdl.handle.net/1805/5503.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Gain-of-function mutations in the KIT receptor tyrosine kinase have been associated with highly malignant human neoplasms. In particular, an acquired somatic mutation at codon 816 in the second catalytic domain of KIT involving an aspartic acid to valine substitution is found in patients with systemic mastocytosis (SM) and acute myeloid leukemia (AML). The presence of this mutation in SM and AML is associated with poor prognosis and overall survival. This mutation changes the conformation of the KIT receptor resulting in altered subs

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