IgE-mediated allergic diseases, including allergic rhinoconjunctivitis and food allergies, are rising in prevalence,1-4 though the mechanisms that govern the persistence of IgE responses continue to remain unidentified. Basophils can mediate allergic effector responses by releasing inflammatory mediators on cross-linking of surface IgE on allergen stimulation. They have also been speculated to play a role in humoral responses in murine models and have been shown to induce IgE production from B cells. We hypothesize that human basophils can induce IgE from human B cells to propagate the allergic response in an IgE and activation dependent manner. Controversy on the origin of persistent IgE production centers on whether IgE is produced by IgE memory B cells originating from germinal centers or results from sequential IgE class switching from IgG producing memory B cells. Basophils have been shown to traffic to lymph nodes, and we hypothesize that basophils can induce IgE production from memory B cells by induction of sequential class switching efficiently. We further speculate that the ability of basophils to endocytose allergen in an IgE mediated fashion may also allow them to present allergens to B cells to propagate an allergen-specific response.

Public Health Relevance

Allergic diseases, including allergic rhinoconjunctivitis and food allergies, are increasing in prevalence in the Unites States, though the mechanisms that govern the persistence of allergy antibodies, or IgE responses, to otherwise harmless substances in the environment continue to remain enigmatic. Basophils, which are allergic effector cells that can release inflammatory chemicals when the IgE on their surface encounters allergens, may have a further role in stimulating IgE antibody production from B cells. We hypothesize that human basophils can stimulate B cells to produce IgE antibodies that can propagate the allergic response, and that the ability of basophils to internalize allergen using their surface IgE may also allow them to present allergens to B cells to propagate an allergen-specific response in allergic individuals.

Agency
National Institute of Health (NIH)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32AI104182-02
Application #
8650653
Study Section
Special Emphasis Panel (ZRG1)
Program Officer
Prograis, Lawrence J
Project Start
Project End
Budget Start
Budget End
Support Year
2
Fiscal Year
2014
Total Cost
Indirect Cost
Name
Massachusetts General Hospital
Department
Type
DUNS #
City
Boston
State
MA
Country
United States
Zip Code
02199
Wong, Johnson T; Ling, Morris; Patil, Sarita et al. (2014) Oxaliplatin hypersensitivity: evaluation, implications of skin testing, and desensitization. J Allergy Clin Immunol Pract 2:40-5