Publication Date:
2019
Description:
〈p〉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 (T〈sub〉H〈/sub〉2)–skewed T follicular helper (T〈sub〉FH〈/sub〉) 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 T〈sub〉FH〈/sub〉 cells and IgE-producing cells in GALT. Food antigen–driven T〈sub〉FH〈/sub〉 cells in GF mice are mostly generated in early life, especially during the weaning period. We also reveal that food antigen–driven T〈sub〉FH〈/sub〉 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.〈/p〉
Electronic ISSN:
2375-2548
Topics:
Natural Sciences in General
