Preventing allergies through the skin

Winslow, Andrew; Keet, Corinne A.

doi:10.1016/j.anai.2022.04.013

Cited by 4 publications

(4 citation statements)

References 58 publications

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“…Epicutaneous immunotherapy (EPIT) is a more novel route of immunotherapy in which the allergen is delivered via a patch on the skin. The possible benefit of this route would be that very small amounts of allergen could be used for desensitization with fewer adverse effects as compared to OIT (36). This route was initially studied in pollen allergy (such as with OIT and SLIT), and has since been studied in well-designed trials for milk and peanut allergy (37)(38)(39)(40)(41)(42)(43).…”

Section: Epicutaneous Immunotherapymentioning

confidence: 99%

Update on clinical research for food allergy treatment

Fowler

Lieberman

2023

Front. Allergy

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The incidence of IgE-mediated food allergy (FA) has continued to increase over the years which places substantial burden on patient health and quality of life. With no cure for this disease, the mainstay of management has been allergen avoidance. However, there have been advancements in FA treatment in recent years with multiple clinical trials utilizing novel and innovative therapeutic strategies. A landmark event came in 2020 with the first drug approval for food allergy with the approval of a product for peanut oral immunotherapy. In addition to oral immunotherapy, different delivery systems of immunotherapy (SLIT, EPIT) are being studied in addition to probiotics, biologic agents - used as monotherapy and as an adjunct, and modified allergens has taken place with the hope to further enhance existing therapeutic options. The hope through these continued developments is for therapies to emerge that will provide a more comprehensive benefit to this patient population.

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Section: Epicutaneous Immunotherapymentioning

confidence: 99%

Update on clinical research for food allergy treatment

Fowler

Lieberman

2023

Front. Allergy

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“…Similarly, the incidence of FA was 40% in patients with AD ( 15 ), compared with a rate of 10% in the general population ( 16 ). Severe AD onset or a high serum level of IgE may predispose to atopic march development ( 17 ).…”

Section: The Atopic Marchmentioning

confidence: 99%

Claudin-1 Mediated Tight Junction Dysfunction as a Contributor to Atopic March

Xia

Cao²,

Zheng³

2022

Front. Immunol.

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Atopic march refers to the phenomenon wherein the occurrence of asthma and food allergy tends to increase after atopic dermatitis. The mechanism underlying the progression of allergic inflammation from the skin to gastrointestinal (GI) tract and airways has still remained elusive. Impaired skin barrier was proposed as a risk factor for allergic sensitization. Claudin-1 protein forms tight junctions and is highly expressed in the epithelium of the skin, airways, and GI tract, thus, the downregulation of claudin-1 expression level caused by CLDN-1 gene polymorphism can mediate common dysregulation of epithelial barrier function in these organs, potentially leading to allergic sensitization at various sites. Importantly, in patients with atopic dermatitis, asthma, and food allergy, claudin-1 expression level was significantly downregulated in the skin, bronchial and intestinal epithelium, respectively. Knockdown of claudin-1 expression level in mouse models of atopic dermatitis and allergic asthma exacerbated allergic inflammation, proving that downregulation of claudin-1 expression level contributes to the pathogenesis of allergic diseases. Therefore, we hypothesized that the tight junction dysfunction mediated by downregulation of claudin-1 expression level contributes to atopic march. Further validation with clinical data from patients with atopic march or mouse models of atopic march is needed. If this hypothesis can be fully confirmed, impaired claudin-1 expression level may be a risk factor and likely a diagnostic marker for atopic march. Claudin-1 may serve as a valuable target to slowdown or block the progression of atopic march.

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“…Four articles in this issue explore this concept through different ideas. [1][2][3][4] It is important to remember that prevention can occur at 2 levels: (1) primary: preventing the disease from occurring; or (2) secondary: preventing the progression or worsening of disease (often called disease-modifying). In terms of allergy, the blocking of the atopic march of atopic dermatitis to other atopic diseases (asthma, food allergy, or allergic rhinitis) is secondary prevention, 5,6 whereas preventing food allergy by early introduction of foods is primary prevention.…”

mentioning

confidence: 99%

“…Skin damage activates alarmins, such as thymic stromal lymphopoietin, skewing the reactions to type 2 cytokines and the development of allergy. 9 Therefore, improving the skin barrier presents an interesting barrier to preventing atopic diseases, as explored by Winslow et al 3 In theory, a normal skin barrier would not activate the type 2 response and no response would be seen. It is also known that patients with atopic dermatitis have a different skin microbiome and it favors the development of allergies.…”

mentioning

confidence: 99%

Can we prevent allergies?

Spergel¹

2022

Annals of Allergy, Asthma & Immunology

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Preventing allergies through the skin

Cited by 4 publications

References 58 publications

Update on clinical research for food allergy treatment

Update on clinical research for food allergy treatment

Claudin-1 Mediated Tight Junction Dysfunction as a Contributor to Atopic March

Can we prevent allergies?

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