Single allergen-induced oral tolerance inhibits airway inflammation in conjugated allergen immunized mice

Chien, Chien-Hui; Yu, Hsin-Hui; Chiang, Bor‐Luen

doi:10.1016/j.jaci.2015.04.018

Cited by 16 publications

(21 citation statements)

References 7 publications

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“…Our previous studies reported that splenic B cells have the potential to induce CD4 + CD25 + Foxp3 − Treg cells, which named as Treg-of-B cells, with suppressive function as well as the Peyer’s patches B cells and peritoneal B-1a cells2829303132. Treg-of-B cells have been demonstrated that protected mice from allergic asthma, arthritis, and inflammatory bowel disease2830313233.…”

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confidence: 99%

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Characterization of c-Maf+Foxp3− Regulatory T Cells Induced by Repeated Stimulation of Antigen-Presenting B Cells

Chien

Chen

et al. 2017

Sci Rep

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The role of B cells in the development of CD4+ regulatory T cells has been emphasized recently. Our previous studies have demonstrated that the antigen-presenting splenic B cells converted naïve CD4+CD25− T cells into CD4+CD25+Foxp3− T cells without additional cytokines or chemicals with regulatory activity and that referred to as Treg-of-B cells. The present study further showed that Treg-of-B cells increased the IL-10-producing population, and the expression of c-Maf, inducible T-cell co-stimulator (ICOS) as well as cytotoxic T-lymphocyte-associated protein 4 (CTLA4) after repeated stimulation of B cells in a cell-cell contact-dependent manner. Long-term cultured Treg-of-B cells exerted IL-10 and CTLA4-mediated antigen-specific suppressive activity; moreover, the single antigen-specific Treg-of-B cells inhibited in a non-antigen-specific fashion. In conclusion, these results suggest that repeated stimulation of B cells induced IL-10-producing CD4+Foxp3− regulatory T cells in a contact-dependent manner and these Treg-of-B cells possess IL-10 and CTLA4-dependent suppressive function.

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confidence: 99%

“…Treg-of-B cells have been demonstrated that protected mice from allergic asthma, arthritis, and inflammatory bowel disease2830313233. Peptide-induced antigen-specific Treg-of-B cells and monoclonal antibodies induced non-antigen-specific Treg-of-B cells possessed suppressive function.…”

mentioning

confidence: 99%

Characterization of c-Maf+Foxp3− Regulatory T Cells Induced by Repeated Stimulation of Antigen-Presenting B Cells

Chien

Chen

et al. 2017

Sci Rep

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“…Reichardt et al demonstrated that Treg-of-B cells potently suppress cutaneous hypersensitivity and ectopic allogeneic heart transplant rejection6. Our group has also demonstrated that Treg-of-B cells induced by splenic B-2 and Peyer’s patch B cells modulated airway inflammation in the murine model of allergic asthma727. The present study examined the function of Treg-of-B cells in a T cell-mediated colitis model.…”

Section: Discussionmentioning

confidence: 73%

“…Treg-of-B cells could suppress the rejection of allogenic heart transplants and also alleviate asthma symptoms67. We demonstrated that splenic B cells and peritoneal B-1a cells as well as Peyer’s patch B cells induced Treg-of-B cells that have many Treg-associated features, such as the production of IL-10 and the expression of CD25, cytotoxic T lymphocyte antigen 4 (CTLA4), inducible costimulator (ICOS), OX40 (CD134), programmed death-1 (PD-1), glucocorticoid-induced tumor necrosis factor receptor (GITR), and LAG378927. Although the characteristics of Treg-of-B cells was very similar to Tr1 cells, Treg-of-B cells did not express CD49b or CD103, two integrin proteins commonly detected in Tr1 cells8.…”

mentioning

confidence: 99%

Novel Foxp3− IL-10− Regulatory T-cells Induced by B-Cells Alleviate Intestinal Inflammation in Vivo

Shao

Hsu

Chien

et al. 2016

Sci Rep

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Recent studies have revealed various Foxp3− regulatory T (Treg) cell subsets effectively protect mice from colitis. In the present study, we demonstrated that B cells induced a particular subset of regulatory T (Treg-of-B) cells, expressing programmed cell death 1 (PD-1), inducible costimulator (ICOS), lymphocyte-activation gene 3 (LAG3), glucocorticoid-induced tumor necrosis factor receptor (GITR), and OX-40, did not express Foxp3. Treg-of-B cells produced abundant levels of IL-10 and low levels of IL-4 and TGF-β. Adoptive transfer of Treg-of-B cells protected mice from CD4+CD45RBhi T-cell-induced colitis, including infiltration of leukocytes, depletion of goblet cells, epithelial hyperplasia, and inhibition of Th1 and Th17 cytokines. These features were similar to IL-10-producing type 1 regulatory T (Tr1) cells; however, IL-10-deficient Treg-of-B cells maintained their suppressive function in vitro as well as in vivo, while the regulation of Tr1 cells depended on IL-10. In conclusion, Treg-of-B cells protected against experimental colitis through an IL-10-independent mechanism. We reported a novel subpopulation of regulatory T cells was different from conventional Foxp3+ Treg and IL-10-producing Tr1 cells.

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“…Furthermore, the results of an animal study conducted by Chiang showed that the preventive oral administration of ovalbumin (OVA) protected β-lactoglobulin (BLG)-conjugated-OVA (B-O)-sensitized mice from BLG-induced airway hyper-responsiveness. The study revealed that non-antigen-specific effect of oral tolerance could be applied as an immunotherapy for allergic disease if the mechanism could be investigated further [69].…”

Section: Induce Immune Tolerance To Allergensmentioning

confidence: 99%

Potential Treatments for Atopic Dermatitis

Kao¹,

Shieh²,

Lee³

et al. 2016

J immuno Biol

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Atopic Dermatitis (AD) is the most common pruritic inflammatory skin disease which causes economic and social burden. AD is not curable and therapeutic options are limited. Currently, the therapeutic approaches to AD include topical treatment, phototherapy, and systemic treatment. Although traditional therapeutic strategies are efficacious in ameliorating the symptoms of AD in most patients, sometimes it is a tough challenge for physicians as AD is catastrophic and difficult to treat. Several potential treatments for AD are being studied owing to a clearer understanding of its pathogenesis. Additionally, animal models of AD allow comprehensive and thorough investigation of pathogenesis and provide more options of therapeutic interventions. The purpose of non-classical treatment strategies for AD is to decrease skin inflammation, re-direct the imbalanced immune polarization, and induce immune tolerance to allergens. Generally, the intervention for mouse model of AD can be classified into 1) monoclonal antibodies, 2) anti-oxidants, 3) allergen-specific immunotherapy, 4) herbal medicine, 5) treatment with materials extracted from food or micronutrients, 6) microbiota/probiotics, 7) bio-composites films, and 8) others. Since half of the patients with AD lack specific immunoglobulin E against allergens, the pathogenesis of different phenotypes still needs to be clarified. Through novel therapies such as cytokine-targeting therapy, miRNA or suppression of thymic stromal lymphopoietin, patients with AD could have better quality of life with less morbidity.

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Single allergen-induced oral tolerance inhibits airway inflammation in conjugated allergen immunized mice

Cited by 16 publications

References 7 publications

Characterization of c-Maf+Foxp3− Regulatory T Cells Induced by Repeated Stimulation of Antigen-Presenting B Cells

Characterization of c-Maf+Foxp3− Regulatory T Cells Induced by Repeated Stimulation of Antigen-Presenting B Cells

Novel Foxp3− IL-10− Regulatory T-cells Induced by B-Cells Alleviate Intestinal Inflammation in Vivo

Potential Treatments for Atopic Dermatitis

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