Journal
MUCOSAL IMMUNOLOGY
Volume 14, Issue 3, Pages 640-651Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/s41385-020-00358-3
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Funding
- Ministry of Education, Culture, Sports, Science, and Technology for Translational Research Network Program (at the University of Tokyo)
- Japan Society for the Promotion of Science [18H05280, 19H03450, 16H06243, 17K19550, 19K22634]
- Funds for the Promotion of Joint International Research [18KK0432]
- Science and Technology Research Partnership for Sustainable Development
- Institute of Medical Science, University of Tokyo
- Senri Life Science Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Takeda Science Foundation
- Uehara Memorial Foundation
- Sumitomo Foundation
- Naito Foundation
- Kato Memorial Bio-Science Foundation
- Yakult Bio-Science Foundation
- NipponHam Foundation
- Chiba University -UC San Diego Center for Mucosal Immunology, Allergy, and Vaccines
- Japan Agency for Medical Research and Development [20gm6010012h0004, 20gm6210024h0001]
- Grants-in-Aid for Scientific Research [19H03450, 19K22634, 18H05280, 17K19550, 16H06243] Funding Source: KAKEN
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Oral immunotherapy (OIT) is an effective approach to controlling food allergy, but the detailed mechanisms are still unknown. Research has shown that desensitization modulates the activation of mast cells, leading to enhanced expansion of regulatory T cells and promotion of clinical allergic unresponsiveness.
Oral immunotherapy (OIT) is an effective approach to controlling food allergy. Although the detailed molecular and cellular mechanisms of OIT are unknown currently, they must be understood to advance the treatment of allergic diseases in general. To elucidate the mechanisms of OIT, especially during the immunological transition from desensitization to allergy regulation, we generated a clinical OIT murine model and used it to examine immunological events of OIT. We found that in mice that completed OIT successfully, desensitized mast cells (MCs) showed functionally beneficial alterations, such as increased induction of regulatory cytokines and enhanced expansion of regulatory T cells. Importantly, these regulatory-T-cell-mediated inhibitions of allergic responses were dramatically decreased in mice lacking OIT-induced desensitized MC. Collectively, these findings show that the desensitization process modulates the activation of MCs, leading directly to enhanced induction of regulatory-T-cell expansion and promotion of clinical allergic unresponsiveness. Our results suggest that efficiently inducing regulatory MCs is a novel strategy for the treatment of allergic disease.
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