Food antigens drive spontaneous IgE elevation in the absence of commensal microbiota
Immunoglobulin E (IgE), a key mediator in allergic diseases, is spontaneously elevated in mice with disrupted commensal microbiota such as germ-free (GF) and antibiotics-treated mice. However, the underlying mechanisms for aberrant IgE elevation are still unclear. Here, we demonstrate that food antigens drive spontaneous IgE elevation in GF and antibiotics-treated mice by generating T helper 2 (TH2)-skewed T follicular helper (TFH) cells in gut-associated lymphoid tissues (GALTs). In these mice, depriving contact with food antigens results in defective IgE elevation as well as impaired generation of TFH cells and IgE-producing cells in GALT. Food antigen-driven TFH cells in GF mice are mostly generated in early life, especially during the weaning period. We also reveal that food antigen-driven TFH cells in GF mice are actively depleted by colonization with commensal microbiota. Thus, our findings provide a possible explanation for why the perturbation of commensal microbiota in early life increases the occurrence of allergic diseases.
|ISBN||2375-2548 (Electronic) 2375-2548 (Linking)|
|Authors||Hong, S. W.; O, E.; Lee, J. Y.; Lee, M.; Han, D.; Ko, H. J.; Sprent, J.; Surh, C. D.; Kim, K. S.|
|Responsible Garvan Author|
|Publisher Name||Science Advances|
|URL link to publisher's version||https://www.ncbi.nlm.nih.gov/pubmed/31131325|