Allergen sensitization stratifies IL-31 production by memory T cells in atopic dermatitis patients

Background:The role of allergen sensitization in IL-31 production by T cells and specifically in the clinical context of atopic dermatitis (AD) has not been characterized. MethodsThe response to house dust mite (HDM) in purified memory T cells cocultured with epidermal cells from AD patients (n=58)...

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Detalhes bibliográficos
Autores: Sans de San Nicolàs, Lídia, Figueras Nart, Ignasi, García-Jiménez, Irene, Bonfill Ortí, Montserrat, Guilabert, Antonio, Curto Barredo, Laia, Bertolín Colilla, Marta, Ferran, Marta, Serra Baldrich, Esther, Pujol, Ramon M., Santamaria Babí, Luis F.
Formato: artículo
Estado:Versión publicada
Fecha de publicación:2023
País:España
Recursos:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/197180
Acesso em linha:https://hdl.handle.net/2445/197180
Access Level:acceso abierto
Palavra-chave:Dermatitis atòpica
Al·lèrgens
Citocines
Cèl·lules T
Atopic dermatitis
Allergens
Cytokines
T cells
Descrição
Resumo:Background:The role of allergen sensitization in IL-31 production by T cells and specifically in the clinical context of atopic dermatitis (AD) has not been characterized. MethodsThe response to house dust mite (HDM) in purified memory T cells cocultured with epidermal cells from AD patients (n=58) and control subjects (n=11) was evaluated. AD-associated cytokines from culture supernatants, plasma proteins and mRNA expression from cutaneous lesions were assessed and related with the clinical features of the patients. ResultsHDM-induced IL-31 production by memory T cells defined two subsets of AD patients according to the presence or absence of IL-31 response. Patients in the IL-31 producing group showed a more inflammatory profile, and increased HDM-specific (sp) and total IgE levels compared to the IL-31 non-producing group. A correlation between IL-31 production and patient's pruritus intensity, plasma CCL27 and periostin was detected. When the same patients were analyzed based on sp IgE and total IgE levels, an increased IL-31 in vitro response, as well as type 2 markers in plasma and cutaneous lesions, was found in patients with sp IgE levels > 100 kUA/L and total IgE levels > 1000 kU/L. The IL-31 response by memory T cells was restricted to the cutaneous lymphocyte-associated antigen (CLA)(+) T-cell subset. ConclusionIgE sensitization to HDM allows stratifying IL-31 production by memory T cells in AD patients and relating it to particular clinical phenotypes of the disease.