Letter to the editor
Single allergen-induced oral tolerance inhibits airway inflammation in conjugated allergen immunized mice

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    In addition, B cells promote Treg expansion to maintain gut homeostasis and suppress colitis (Wang et al., 2015). The adoptive transfer of Treg-of-B cells protects mice from allergic airway hypersensitivity and collagen-induced arthritis (Chen et al., 2016; Chien et al., 2015). Additionally, Treg-of-B cells inhibit Th1/Th17 cytokine production from mesenteric lymph nodes in a colitis mouse model (Shao et al., 2016) and can suppress the proliferation of effector T cells (Chien and Chiang, 2017; Chien et al., 2015; Chu and Chiang, 2012, 2015; Hsu et al., 2014; Reichardt et al., 2007; Waisman et al., 2013; Wang et al., 2015).

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    Our data expand on this study by demonstrating that short peptides administered after sensitization and coupled with coadministration of whole allergen proteins (OVA and Fel d 1) can prevent the development of airway inflammation induced by a distinct, non–cross-reactive allergen. Chien et al53 also investigated the non–antigen-specific effects of immunotherapy by demonstrating that feeding mice OVA after sensitization to β-lactoglobulin–conjugated OVA ameliorated airway inflammation induced by challenge with either OVA or β-lactoglobulin. Our data corroborate the notion that immunotherapy can modulate both specific and non–antigen-specific effects while demonstrating that peptide immunotherapy, a clinically relevant therapy administered in a clinically relevant route, can perform this function.

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    Although IL-2 is also a crucial cytokine for the development of CD4+CD25+ Tregs, it can be inferred that CD4+CD25+LAG3+ Treg-of-B cells have an autocrine system for maintaining viability [28,29]. Tregs from LAG3−/− mice exhibit reduced regulatory activity [32], and LAG3−/− mice exhibit accelerated autoimmune diabetes [33], indicating that LAG3 plays a critical role in preventing autoimmune diseases. We found that LAG3 participated in Treg-of-B-cell-mediated immunosuppression in vitro (Fig. 2C, F).

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This study was supported by the National Science Council (grant no. NSC 101-2314-B-002-064-MY2) and the National Health Research Institute (grant no. NHRI-EX104-1025SI).

Disclosure of potential conflict of interest: The authors declare that they have no relevant conflicts of interest.

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