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Editorial
. 2022 Feb 15;205(4):375-377.
doi: 10.1164/rccm.202110-2322ED.

Mechanisms of Mast Cell Activation in Severe Asthma: Beyond IgE

Peter Bradding  1   2
Affiliations
Editorial

Mechanisms of Mast Cell Activation in Severe Asthma: Beyond IgE

Peter Bradding. Am J Respir Crit Care Med. .
No abstract available

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Figures

Figure 1.
Figure 1.
Examples of ligands and receptors capable of activating human mast cells. Many of these ligands and activating stimuli are active in the airways of people with asthma and therefore likely to contribute to the ongoing mast cell activation evident in asthmatic airways. The downstream signaling pathways for many of these receptors in mast cells and how they interact with each other are not fully understood. Among the well-known signaling pathways are the PLC-γ and PI3K pathways, which mobilize intracellular Ca2+, leading to Ca2+ influx via Orai channels. Modified from Reference . ADDS = antibody-dependent degranulatory synapse; CADM1 = cell adhesion molecule-1; CRH = corticotropin-releasing hormone; CRH-R = CRH receptor; FcR = Fc receptor; IP3 = inositol-1,4,5-triphosphate; LT = leukotriene; MBP = major basic protein; MRGPRX2 = Mas-related G protein–coupled receptor-X2; PAF = platelet-activating factor; PI3K = phosphoinositide 3-kinase; PAR = protease-activated receptor; PGN = peptidoglycan; PLC-γ = phospholipase Cγ; PM10 = particulate matter ⩽10 μm in aerodynamic diameter; R = receptor; SCF = stem cell factor; TLR = Toll-like receptor; TNF = tumor necrosis factor; TSLP = thymic stromal lymphopoietin.
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Comment on

References

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