Abstract：
:Antigen (Ag)-mediated crosslinking of IgE-loaded high-affinity receptors for IgE (FcεRI) on mast cells (MCs) triggers activation of proinflammatory effector functions relevant for IgE-associated allergic disorders. The cytosolic tyrosine kinase BTK and the SH2-containing inositol-5'-phosphatase SHIP1 are central positive and negative regulators of Ag-triggered MC activation, respectively, contrarily controlling Ca2+ mobilisation, degranulation, and cytokine production. Using genetic and pharmacological techniques, we examined whether BTK activation in Ship1-/- MCs is mandatory for the manifestation of the well-known hyperactive phenotype of Ship1-/- MCs. We demonstrate the prominence of BTK for the Ship1-/- phenotype in a manner strictly dependent on the strength of the initial Ag stimulus; particular importance for BTK was identified in Ship1-/- bone marrow-derived MCs in response to stimulation with suboptimal Ag concentrations. With respect to MAPK activation, BTK showed particular importance at suboptimal Ag concentrations, allowing for an analogous-to-digital switch resulting in full activation of ERK1/2 already at low Ag concentrations. Our data allow for a more precise definition of the role of BTK in FcεRI-mediated signal transduction and effector function in MCs. Moreover, they suggest that reduced activation or curtate expression of SHIP1 can be compensated by pharmacological inhibition of BTK and vice versa.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Zorn CN,Simonowski A,Huber Mdoi
10.1038/s41598-018-33769-1subject
Has Abstractpub_date
2018-10-19 00:00:00pages
15467issue
1issn
2045-2322pii
10.1038/s41598-018-33769-1journal_volume
8pub_type
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