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. 2017 Jul 3;7:4534. doi: 10.1038/s41598-017-04890-4

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Differences and commonalities in TLR4- and FcεRI-activated production of proinflammatory cytokines. (a) LPS-induced stimulation of TLR4 in MCs results in activation of the MYD88 pathway. The E3 ligase TRAF6 mediates the activation of the Ser/Thr kinase TAK1, which allows for bifurcation of the signal into the NFκB and MAPK pathways leading to transcription of proinflammatory genes. This is suppressed by inhibition of TAK1 (by Oxo) and IKK-β (by InhIV; CsA inhibits calcineurin, indirectly contributing to suppression of IKK-β^{31, 33}). (b) Ag-induced crosslinking of the IgE-bound FcεRI leads to NFκB activation mediated by the CARMA1/BCL10/MALT1 complex as well as TRAF6 and TAK1^{23, 52}. In contrast to TLR4 signalling, FcεRI triggering leads to PLCγ/IP₃-controlled store-operated Ca²⁺ influx allowing for dephosphorylation/activation of NFAT by Ca²⁺/CaM-activated calcineurin. Whereas CsA directly and indirectly inhibits calcineurin and IKK-β, respectively, INCA6 selectively blocks the interaction of calcineurin and NFAT³⁰.