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Antagonism of the interleukin 4 receptor α promotes T H 1‐signalling among T cells from patients with atopic dermatitis after stimulation
Author(s) -
Brøgger Peter,
Blom Lars H.,
Simonsen Stine,
Thyssen Jacob P.,
Skov Lone
Publication year - 2020
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12835
Subject(s) - immunology , monoclonal antibody , blocking antibody , flow cytometry , atopic dermatitis , stimulation , cytokine , interleukin , interleukin 4 , receptor , medicine , antibody , endocrinology
Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease. Molecular characterization of AD shows an underlying inflammation with tissue infiltration of T helper (T H ) 2 cells and increased IL‐4 and IL‐13. The multifaceted roles of IL‐4 and IL‐13 in allergic disease development make IL‐4Rα an attractive target for treatment strategies, and a neutralizing monoclonal antibody which antagonizes the effects of both IL‐4 and IL‐13 by blocking the interaction site found in the IL‐4 receptor subunit α (IL‐4Rα) has been successfully used to treat patients with moderate‐to‐severe AD. To elucidate the effects of IL‐4Rα blockade on the cellular level, we used flow cytometry to examine cytokine production after antigen stimulation in human T cells from patients with AD (n = 12) and healthy controls (n = 6). The cells were stimulated with and without a neutralizing monoclonal antibody against IL‐4Rα. Our results indicate that blocking IL‐4Rα prohibits IL‐4 signalling and IL‐13 signalling and thereby T H 2 differentiation followed by an upregulation of interferon‐γ‐producing cells.