604:
Detection of antigen-specific IgE-expressing B cells in food allergy is feasible and inversely associated with dietary antigen exposure
Sunday, March 4, 2018: 2:15 PM
S230AB (Convention Center)
Shailesh Choudhary, PhD,
RATIONALE: To understand the regulation of IgE production in the recently described alpha-gal mammalian meat food allergy, we have focused on IgE-expressing (IgE+) B cells. These cells typically circulate in low abundance and are generally difficult to detect. Recent improvements in technical methods have made their analysis more feasible. Once identified, we asked whether circulating alpha-gal-specific IgE+ B cell populations were affected by ongoing dairy consumption as others have shown that B cell receptor (BCR) signaling negatively regulates IgE responses.

METHODS: PBMCs were isolated from controls and subjects with alpha-gal allergy and stained for surface markers CD19, CD38, CD27, CD138, and membrane IgM, IgG, IgD and IgE as well as fluorochrome-labeled alpha-gal.

RESULTS: IgE+B cells that also stained positive for alpha-gal were identified in five subjects allergic to mammalian meat. These alpha-gal-specific IgE+B cells were absent in controls. Of total stained singlet cells, the population of alpha-gal-specific IgE+B cells was 0.092% (median) with a range of 0.013% to 0.15%. There was no association of alpha-gal-specific IgE+B cell frequency with reported severity of allergic reactions. Interestingly, subjects reporting ongoing consumption of alpha-gal antigen in dairy form had generally higher proportion of antigen-specific IgE+B cells.

CONCLUSIONS: We have reproducibly identified circulating antigen-specific IgE+B cells in adult subjects with alpha-gal mammalian meat food allergy. Although BCR signaling is thought to negatively regulate IgE responses, our data suggest ongoing dietary antigen exposure is associated with increased numbers of antigen-specific IgE+B cells. Future studies will track these double-positive B cells longitudinally to assess the impact of additional tick bites.