Letter to the EditorIgE allergen component-based profiling and atopic manifestations in patients with Netherton syndrome
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Cited by (36)
Transcriptomic Analysis of the Major Orphan Ichthyosis Subtypes Reveals Shared Immune and Barrier Signatures
2022, Journal of Investigative DermatologyNetherton syndrome subtypes share IL-17/IL-36 signature with distinct IFN-α and allergic responses
2022, Journal of Allergy and Clinical ImmunologyCitation Excerpt :In addition to skin barrier defect and inflammation, all NS patients studied, except patient 8, had elevated serum IgE levels associated with atopic manifestations. Specific IgE profiling revealed that all NS patients were sensitized to at least 1 panallergen and presented sensitivity to food and airway allergens, as previously shown in a pediatric NS cohort.58 Immunophenotyping of PBMCs revealed increased TH2 subset in NS-ILC, suggesting that the TH2 axis contributes to allergic manifestations in NS-ILC patients.
Skin Microbiota and Clinical Associations in Netherton Syndrome
2021, JID InnovationsGenetics of Food Allergy
2021, Immunology and Allergy Clinics of North AmericaTransgenic Kallikrein 14 Mice Display Major Hair Shaft Defects Associated with Desmoglein 3 and 4 Degradation, Abnormal Epidermal Differentiation, and IL-36 Signature
2020, Journal of Investigative DermatologyEczematous dermatitis in primary immunodeficiencies: A review of cutaneous clues to diagnosis
2020, Clinical ImmunologyCitation Excerpt :Notably, trichorrhexis invaginata can be a late manifestation of NS, leading to a delay in diagnosis [32,57,61]. Atopy is also a reliable feature of NS; a study of atopic symptoms in 10 Finnish patients diagnosed with NS demonstrated multiple allergies (eggs, cow's milk, wheat, nuts and pollens), increased serum total IgE levels, and hypereosinophilia [62]. Urticaria, asthma and angioedema were also commonly seen in these patients [62].
Supported by Helsinki University Hospital Research funds (grant no. TYH2013235).
Disclosure of potential conflict of interest: K. Hannula-Jouppi has been supported by Helsinki University Hospital Research Funds (grant no. TYH2013235), has received travel support from the Finnish Dermatology Society, and has received travel support from the Finnish Dermatology Society and Jannsen-Cilaq. N. Kluger has been supported by grant the Helsinki University Central Hospital Research Funds (grant no. TYH2013235). S. Mäkinen-Kiljunen has received consultancy fees, lecture fees, and travel support from Thermo Fisher Scientific. A. Ranki is a member of the Independent Data Monitoring Committee, Millennium Pharmaceuticals, and the ImmunoQure AG Advisory Board. The rest of the authors declare that they have no relevant conflicts of interest.