Stat5B is required for IgE-Mediated mast cell function in vitro and in vivo

Mast cells are found primarily at interfaces with the external environment, where they provide protection from pathogens but also elicit allergic inflammation. Mast cell activation by antigen-induced aggregation of IgE bound to the high affinity receptor, FcERI, is a critical factor leading to inflammation and bronchoconstriction. We previously found that Stat5 is activated by FcERI and that Stat5B suppression decreased IgE-induced cytokine production in vitro, but in vivo responses have not been assessed. We now show that Stat5B-deficient (KO) mice have reduced responses to IgE-mediated anaphylaxis, despite normal mast cell tissue distribution. Similarly, Stat5B KO mast cells have diminished IgE-induced degranulation and cytokine secretion in vitro. These mice have elevated IgE production that is not correlated with an intrinsic B cell defect. The current work demonstrates that the Stat5B isoform is required for normal mast cell function and suggests it limits IgE production in vivo.

Automated summary

The lack of Stat5B in mice results in reduced responses to IgE-mediated anaphylaxis and diminished IgE-induced degranulation and cytokine secretion in mast cells. These findings suggest that the Stat5B isoform is crucial for normal mast cell function and may play a role in limiting IgE production in vivo.