Increasing evidence supports the proposal of a role for commensal microorganisms in shaping systemic immune responses. In Nature Medicine, Artis and colleagues show that commensal bacteria can suppress the switching of B cells to immunoglobulin E (IgE). Germ-free mice and mice treated with broad-spectrum antibiotics have higher concentrations of circulating IgE. In turn, higher IgE concentrations correlate with more basophils and T helper type 2 cells and skewing toward type 2 immune responses in these mice. IgE induces upregulation of the receptor for IL-3 (CD123) in bone marrow precursor cells, which results in more basophil progenitor cells. Inhibition of IgE production or blockade of the receptor FceRIa diminishes the basophilia of the antibiotic-treated mice. Intriguingly, B cell–intrinsic expression of the adaptor MyD88 suppresses IgE production, basophilia and enhanced susceptibility to atopic disease. These findings may explain the greater incidence of atopic diseases as a result of more antibiotic use.

Nat. Med. 18, 538–546 (2012)