IgE sensitization in relation to preschool eczema and filaggrin mutation

Johansson, Emma; Bergström, Anna; Kull, Inger; Lind, Tomas; Söderhäll, Cilla; Hage, Marianne van; Wickman, Magnus; Ballardini, Natalia; Wahlgren, Carl-Fredrik

doi:10.1016/j.jaci.2017.04.008

Cited by 39 publications

(32 citation statements)

References 34 publications

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“…Previous studies have found that children that carry a FLG mutation have an increased risk of peanut allergy even after adjusting for eczema . In this study, eczema seemed to be the overriding factor for peanut sensitization; however, it should be noted that FLG mutations were quite low in BAMSE (7.14%) in comparison with other population‐based cohorts . Tree nut and/or soya allergy by age 8 was also associated with primary peanut sensitization at age 8 years; co‐existent peanut and tree nut allergy have been shown in numerous studies, whereas co‐existent soya and peanut allergy are reportedly low in other populations …”

Section: Discussioncontrasting

confidence: 57%

Environmental peanut exposure increases the risk of peanut sensitization in high‐risk children

Brough

Kull

Richards

et al. 2018

Clin Experimental Allergy

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Section: Discussioncontrasting

confidence: 57%

Environmental peanut exposure increases the risk of peanut sensitization in high‐risk children

Brough

Kull

Richards

et al. 2018

Clin Experimental Allergy

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“…The phenotype, genotype, and mouse models have all recently been reviewed [185, 187-190]. In addition, filaggrin ( FLG ) deficiency can lead to impaired keratinization and defective skin barriers, which result in ichthyosis vulgaris and in some patients with elevated serum IgE [191-193]. It is usually categorized as an inherited disorder of keratinization.…”

Section: Other Syndromes In Which Ige Levels Are Highmentioning

confidence: 99%

Human hyper-IgE syndrome: singular or plural?

et al. 2018

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Spectacular progress has been made in the characterization of human hyper-IgE syndrome (HIES) over the last 50 years. HIES is a primary immunodeficiency defined as an association of atopy in a context of very high serum IgE levels, characteristic bacterial and fungal diseases, low-level clinical and biological inflammation, and various non-hematopoietic developmental manifestations. Somewhat arbitrarily, three disorders were successively put forward as the underlying cause of HIES: autosomal dominant (AD) STAT3 deficiency, the only disorder corresponding to the original definition of HIES, and autosomal recessive (AR) DOCK8 and PGM3 deficiencies, in which atopy and high serum IgE levels occur in a context of manifestations not seen in patients with typical HIES. Indeed, these three disorders disrupt different molecular pathways, affect different cell types, and underlie different clinical phenotypes. Surprisingly, several other inherited inborn errors of immunity in which serum IgE levels are high, sometimes almost as high as those in HIES patients, are not considered to belong to the HIES group of diseases. Studies of HIES have been further complicated by the lack of a high serum IgE phenotype in all mouse models of the disease other than two Stat3 mutant strains. The study of infections in mutant mice has helped elucidate only some forms of HIES and infection. Mouse models of these conditions have also been used to study non-hematopoietic phenotypes for STAT3 deficiency, tissue-specific immunity for DOCK8 deficiency, and cell lineage maturation for PGM3 deficiency. We review here the history of the field of HIES since the first clinical description of this condition in 1966, together with the three disorders commonly referred to as HIES, focusing, in particular, on their mouse models. We propose the restriction of the term "HIES" to patients with an AD STAT3-deficiency phenotype, including the most recently described AR ZNF341 deficiency, thus excluding AR DOCK8 and PGM3 deficiencies from the definition of this disease.

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“…Moreover, food allergy, oral allergy syndrome, and eosinophilic esophagitis are commonly associated with AD [116]. There is evidence that the skin might be the starting point of the atopic march, i.e., (1) mutations in filaggrin, a key barrier protein, have been reported to be associated with severe eczema and bronchial asthma as well as food allergy [117, 118], and (2) epicutaneous sensitization to proteins (food and pollen) paves the way for developing food allergy and airway allergic diseases [119-121]. …”

Section: Pathogenenic Mechanismsmentioning

confidence: 99%

Atopic Dermatitis: Collegium Internationale Allergologicum (CIA) Update 2019

Simon

Wollenberg

Renz

et al. 2019

Int Arch Allergy Immunol

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Atopic dermatitis (AD) is a chronic inflammatory skin disease presenting with recurrent eczematous lesions and intense pruritus. It is common and affects both children and adults, often beginning in infancy. Due to the unpredictable disease course, its visible skin lesions, itching and scratching followed by sleeplessness, other associated atopic diseases, and behavioral and psychiatric disorders, AD is an immense burden for patients and caregivers. AD is determined by a genetic predisposition characterized by an impaired skin barrier and a T-helper-2-predominant inflammation. Restoration of the skin barrier is the main approach for treating and preventing AD. In order to cope with acute flares, usually topical corticosteroids (TCS) are applied, while topical calcineurin inhibitors (TCI) are used mainly for maintenance therapy. There is a small group of patients who are refractory to TCS and TCI and require systemic immunosuppressive drugs such as ciclosporin. Novel, targeted therapies are under clinical investigation, among which an anti-IL-4/IL-13 receptor antibody has recently been approved in several countries. As we learn to understand the pathomechanisms of AD, the characteristics of the different patient subgroups, and the effectiveness of various targeted therapies, a personalized treatment ensuring the best efficacy and safety and, probably, a disease-modifying effect will result.

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IgE sensitization in relation to preschool eczema and filaggrin mutation

Abstract: PSE is associated with IgE sensitization to both food allergens and aeroallergens up to 16 years of age. FLG mutation is associated with IgE sensitization to peanut but not to other allergens. Sensitized children with preceding PSE are more often polysensitized.

Cited by 39 publications

References 34 publications

Environmental peanut exposure increases the risk of peanut sensitization in high‐risk children

Environmental peanut exposure increases the risk of peanut sensitization in high‐risk children

Human hyper-IgE syndrome: singular or plural?

Atopic Dermatitis: Collegium Internationale Allergologicum (CIA) Update 2019

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