Please use this identifier to cite or link to this item: https://doi.org/10.1172/JCI87492
Title: Mast cell desensitization inhibits calcium flux and aberrantly remodels actin
Authors: Gladys Ang, W.X
Church, A.M
Kulis, M
Choi, H.W
Wesley Burks, A
Abraham, S.N 
Keywords: actin
antigen
calcium
Fc receptor
immunoglobulin E
immunoglobulin E receptor
silver
actin
immunoglobulin E
immunoglobulin E receptor
actin filament
anaphylaxis
animal cell
animal experiment
animal model
antigen specificity
Article
calcium transport
cell surface
controlled study
desensitization
female
in vitro study
mast cell
mast cell degranulation
mouse
nonhuman
priority journal
anaphylaxis
animal
calcium signaling
CHO cell line
Cricetulus
degranulation
disease model
hamster
immunology
mast cell
pathology
signal transduction
Actin Cytoskeleton
Actins
Anaphylaxis
Animals
Calcium Signaling
Cell Degranulation
CHO Cells
Cricetinae
Cricetulus
Disease Models, Animal
Immunoglobulin E
Mast Cells
Mice
Receptors, IgE
Signal Transduction
Issue Date: 2016
Publisher: American Society for Clinical Investigation
Citation: Gladys Ang, W.X, Church, A.M, Kulis, M, Choi, H.W, Wesley Burks, A, Abraham, S.N (2016). Mast cell desensitization inhibits calcium flux and aberrantly remodels actin. Journal of Clinical Investigation 126 (11) : 4103-4118. ScholarBank@NUS Repository. https://doi.org/10.1172/JCI87492
Rights: Attribution 4.0 International
Abstract: Rush desensitization (DS) is a widely used and effective clinical strategy for the rapid inhibition of IgE-mediated anaphylactic responses. However, the cellular targets and underlying mechanisms behind this process remain unclear. Recent studies have implicated mast cells (MCs) as the primary target cells for DS. Here, we developed a murine model of passive anaphylaxis with demonstrated MC involvement and an in vitro assay to evaluate the effect of DS on MCs. In contrast with previous reports, we determined that functional IgE remains on the cell surface of desensitized MCs following DS. Despite notable reductions in MC degranulation following DS, the high-affinity IgE receptor FcμRI was still capable of transducing signals in desensitized MCs. Additionally, we found that displacement of the actin cytoskeleton and its continued association with FcμRI impede the capacity of desensitized MCs to evoke the calcium response that is essential for MC degranulation. Together, these findings suggest that reduced degranulation responses in desensitized MCs arise from aberrant actin remodeling, providing insights that may lead to improvement of DS treatments for anaphylactic responses.
Source Title: Journal of Clinical Investigation
URI: https://scholarbank.nus.edu.sg/handle/10635/179279
ISSN: 0021-9738
DOI: 10.1172/JCI87492
Rights: Attribution 4.0 International
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