Original Research Paper

Inflammation Research

, Volume 59, Issue 3, pp 207-218

First online:

IL-33 synergizes with IgE-dependent and IgE-independent agents to promote mast cell and basophil activation

  • Matthew R. SilverAffiliated withInflammation Research, WyethCell Signaling Technology
  • , Alexander MargulisAffiliated withInflammation Research, WyethGenzyme
  • , Nancy WoodAffiliated withInflammation Research, Wyeth
  • , Samuel J. GoldmanAffiliated withInflammation Research, Wyeth
  • , Marion KasaianAffiliated withInflammation Research, Wyeth
  • , Divya ChaudharyAffiliated withInflammation Research, Wyeth Email author 

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Mast cell and basophil activation contributes to inflammation, bronchoconstriction, and airway hyperresponsiveness in asthma. Because IL-33 expression is inflammation inducible, we investigated IL-33-mediated effects in concert with both IgE-mediated and IgE-independent stimulation.


Because the HMC-1 mast cell line can be activated by GPCR and RTK signaling, we studied the effects of IL-33 on these pathways. The IL-33- and SCF-stimulated HMC-1 cells were co-cultured with human lung fibroblasts and airway smooth muscle cells in a collagen gel contraction assay. IL-33 effects on IgE-mediated activation were studied in primary mast cells and basophils.


IL-33 synergized with adenosine, C5a, SCF, and NGF receptor activation. IL-33-stimulated and SCF-stimulated HMC-1 cells demonstrated enhanced collagen gel contraction when cultured with fibroblasts or smooth muscle cells. IL-33 also synergized with IgE receptor activation of primary human mast cells and basophils.


IL-33 amplifies inflammation in both IgE-independent and IgE-dependent responses.


ST2 signaling HMC-1 IgE receptor Adenosine receptors RTK signaling