| Literature DB >> 31027995 |
Juan-Manuel Leyva-Castillo1, Claire Galand1, Christy Kam1, Oliver Burton1, Michael Gurish2, Melissa A Musser3, Jeffrey D Goldsmith4, Elizabeth Hait5, Samuel Nurko5, Frank Brombacher6, Chen Dong7, Fred D Finkelman8, Richard T Lee9, Steven Ziegler10, Isaac Chiu3, K Frank Austen2, Raif S Geha11.
Abstract
Mast cell (MC) mediator release after crosslinking of surface-bound IgE antibody by ingested antigen underlies food allergy. However, IgE antibodies are not uniformly associated with food allergy, and intestinal MC load is an important determinant. Atopic dermatitis (AD), characterized by pruritis and cutaneous sensitization to allergens, including foods, is strongly associated with food allergy. Tape stripping mouse skin, a surrogate for scratching, caused expansion and activation of small intestinal MCs, increased intestinal permeability, and promoted food anaphylaxis in sensitized mice. Tape stripping caused keratinocytes to systemically release interleukin-33 (IL-33), which synergized with intestinal tuft-cell-derived IL-25 to drive the expansion and activation of intestinal type-2 innate lymphoid cells (ILC2s). These provided IL-4, which targeted MCs to expand in the intestine. Duodenal MCs were expanded in AD. In addition to promoting cutaneous sensitization to foods, scratching may promote food anaphylaxis in AD by expanding and activating intestinal MCs.Entities:
Keywords: ILC2s; food allergy; gut; innate immunity; mast cells; skin
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Year: 2019 PMID： 31027995 PMCID： PMC6531322 DOI： 10.1016/j.immuni.2019.03.023
Source DB: PubMed Journal: Immunity ISSN： 1074-7613 Impact factor: 31.745