2012
DOI: 10.1016/j.jaci.2012.04.039
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Early suppression of basophil activation during allergen-specific immunotherapy by histamine receptor 2

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Cited by 125 publications
(108 citation statements)
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“…Although AIT reduces the allergic inflammation mediated by IgE-dependent mechanism over the time, a very early effect on basophil and mast cell activation status is observed just after the initiation of the therapeutic regimen, leading to a lower risk to develop anaphylactic manifestations [33][34][35]. The subjacent mechanism of basophil and mast cell desensitization has not been elucidated yet; however, some clues highlight this issue.…”
Section: Cellular and Molecular Mechanisms Of Aitmentioning
confidence: 99%
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“…Although AIT reduces the allergic inflammation mediated by IgE-dependent mechanism over the time, a very early effect on basophil and mast cell activation status is observed just after the initiation of the therapeutic regimen, leading to a lower risk to develop anaphylactic manifestations [33][34][35]. The subjacent mechanism of basophil and mast cell desensitization has not been elucidated yet; however, some clues highlight this issue.…”
Section: Cellular and Molecular Mechanisms Of Aitmentioning
confidence: 99%
“…The levels of mRNA and FcεRI cell-surface expression decreased in basophil cells from patients submitted to venom immunotherapy, indicating that the reduction in FcεRI expression contributes to the phenomenon of the early basophil desensitization observed after AIT [37,38]. On the other hand, AIT also provokes an allergen-mediated upregulation of the type 2 histamine receptor (H2R) gene, which was associated with the suppression of FcεRI-mediated basophil activation, inducing a tolerogenic response (Figure 2) [34,39]. The engagement of H2R with its agonists prevents further histamine and leukotriene releasing as well as IL-4 and IL-8 production by basophil cells [34].…”
Section: Cellular and Molecular Mechanisms Of Aitmentioning
confidence: 99%
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“…Several hypotheses to explain the mechanisms underlying cell hyporesponsiveness were proposed, such as exhaustion of stored mediators caused by repetitive stimulation (taquiphylaxis), Syk and Lyn consumption, FceRI internalization, activation of inhibitory receptors, and suboptimal doses of antigen unable to cross-link FceRI receptors. It has been established that activating signals are counterbalanced by inhibition signals and a number of inhibitory receptors have been identified on mast cells [8][9][10][11]. Some of these, such as FcγRII and LILRB4 (GP49), are immunoreceptors signalizing throw tyrosine-based inhibitory motifs (ITIMs) that recruit protein tyrosine phosphatases, which are negative regulators of FceRI-mediated mast cell responses [12].…”
Section: Introductionmentioning
confidence: 99%