Mechanical Skin Injury Promotes Food Anaphylaxis by Driving Intestinal Mast Cell Expansion

Leyva-Castillo, Juan-Manuel; Galand, C; Kam, Christy; Burton, Oliver T.; Gurish, Michael F.; Musser, Melissa A.; Goldsmith, Jeffrey D.; Hait, Elizabeth J.; Nurko, Samuel; Brombacher, Frank; Dong, Chen; Finkelman, Fred D.; Lee, Richard T.; Ziegler, Steven F.; Chiu, Isaac M.; Austen, K. Frank

doi:10.1016/j.immuni.2019.03.023

Cited by 179 publications

(153 citation statements)

References 50 publications

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“…6). It has been reported that the expansion of intestinal mast cells elicited by mechanical skin injury promotes oral anaphylaxis [39]. Therefore, our results suggest that the degranulation of intestinal mast cells could be weakened by oral administration of gliadin or peptic-GLI, leading to the suppression of anaphylactic responses.…”

Section: Discussionmentioning

confidence: 51%

Induction of Oral Tolerance by Pepsin-Digested Gliadin Retaining T Cell Reactivity in a Mouse Model of Wheat Allergy

Miyakawa

Takano

et al. 2020

Int Arch Allergy Immunol

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Background: Wheat is known as the most widely consumed food all over the world. Although many types of wheat allergy have been recognized, their treatment still has a long way to go due to the complex pathogenesis. Oral immunotherapy (OIT) is under investigation for the treatment of wheat allergies. Previous studies have demonstrated that OIT using intact wheat allergens can induce tolerance, but is accompanied by a high risk of anaphylactic reactions. Objectives: Our objective was to prepare modified wheat allergens with hypoallergenic and tolerance-inducing properties to reduce adverse effects during immunotherapy. Methods: Wheat gliadin was degraded by hydrolysis with pepsin and trypsin, and then the hydrolysate was deamidated with hydrochloric acid. The IgE-binding capacity and T cell reactivity of the degraded gliadins were evaluated in vitro. Pepsin-di-gested gliadin (peptic-GLI) was applied in a mouse model to investigate whether it would induce oral tolerance. Results: Degradation with pepsin decreased IgE-binding capacity and maintained T cell reactivity. Oral administration of peptic-GLI to mice before sensitization and challenge with gliadin could significantly suppress the production of IgE, IgG1, and type 2 T helper cytokines. Moreover, the development of anaphylactic reactions and allergic responses of the small intestine induced by gliadin challenge were inhibited by oral administration of peptic-GLI. Conclusions: The findings of this study indicate that peptic-GLI with low allergenicity and potential for tolerance induction may become useful in wheat immunotherapy with less adverse effects.

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Section: Discussionmentioning

confidence: 51%

Induction of Oral Tolerance by Pepsin-Digested Gliadin Retaining T Cell Reactivity in a Mouse Model of Wheat Allergy

Miyakawa

Takano

et al. 2020

Int Arch Allergy Immunol

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“…The characterization of subpopulations of mast cells by single-cell RNA-seq, together with analysis of encoded proteins, will be of paramount importance to modulate the injury-or repair-inducing abilities of these immune cells.] For several decades mast cells were considered to play mainly proinflammatory roles in several allergic disorders, such as bronchial asthma [2][3][4]122], allergic rhinitis [5], urticaria [6,7], food allergy [8,9], anaphylaxis [10,11], atopic dermatitis [12], and angioedema [13]. During the last years, it became evident that mast cells represent an important cell during bacterial [26,27,29], fungal [29], viral [25,29], and helminth infections [30,31].…”

Section: Discussionmentioning

confidence: 99%

“…At that time, the mast cells' distinguishing feature was the affinity of their cytoplasmic granules for certain basic dyes. For several decades, mast cells and their mediators were essentially considered to play mainly a proinflammatory role in allergic disorders, such as bronchial asthma [2][3][4], allergic rhinitis [5], urticaria [6,7], food allergy [8,9], anaphylaxis [10,11], atopic dermatitis [12], and angioedema [13]. With the appreciation of these cells as major potential sources of a myriad of cytokines and chemokines, it became evident in the 1990s that mast cells may express immunoregulatory functions [14,15].…”

mentioning

confidence: 99%

Mast Cells: Fascinating but Still Elusive after 140 Years from Their Discovery

Varricchi

Marone

2020

IJMS

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“…to crosslink IgE-bound FcεRI to activate intestinal mast cells and basophils to elicit the food allergy phenotype (Figure 2). [44]. These cytokines initiate a Th2-skewed immune response.…”

Section: Hrf In Allergic and Immune Diseasesmentioning

confidence: 99%

Histamine-Releasing Factor, a New Therapeutic Target in Allergic Diseases

Kawakami

Kasakura

Kawakami

2019

Cells

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Histamine-releasing activities on human basophils have been studied as potential allergy-causing agents for four decades. An IgE-dependent histamine-releasing factor (HRF) was recently shown to interact with a subset of immunoglobulins. Peptides or recombinant proteins that block the interactions between HRF and IgE have emerged as promising anti-allergic therapeutics, as administration of them prevented or ameliorated type 2 inflammation in animal models of allergic diseases such as asthma and food allergy. Basic and clinical studies support the notion that HRF amplifies IgE-mediated activation of mast cells and basophils. We discuss how secreted HRF promotes allergic inflammation in vitro and in vivo complex disease settings.

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Mechanical Skin Injury Promotes Food Anaphylaxis by Driving Intestinal Mast Cell Expansion

Cited by 179 publications

References 50 publications

Induction of Oral Tolerance by Pepsin-Digested Gliadin Retaining T Cell Reactivity in a Mouse Model of Wheat Allergy

Induction of Oral Tolerance by Pepsin-Digested Gliadin Retaining T Cell Reactivity in a Mouse Model of Wheat Allergy

Mast Cells: Fascinating but Still Elusive after 140 Years from Their Discovery

Histamine-Releasing Factor, a New Therapeutic Target in Allergic Diseases

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