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Administration of anti‐interleukin 18 antibody fails to inhibit development of dermatitis in atopic dermatitis‐model mice NC/Nga
Author(s) -
Higa S.,
Kotani M.,
Matsumoto M.,
Fujita A.,
Hirano T.,
Suemura M.,
Kawase I.,
Tanaka T.
Publication year - 2003
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.2003.05406.x
Subject(s) - atopic dermatitis , immunoglobulin e , immunology , scratching , medicine , antibody , interleukin , histamine , exacerbation , cytokine , pharmacology , physics , acoustics
Summary Background Interleukin (IL)‐18 has been shown to activate basophils to produce histamine and IL‐4 and to induce naive T cells to differentiate into T‐helper (Th) 2 cells. However, when expressed together with IL‐12, IL‐18 induces Th1 cell development and inhibits IgE synthesis. Previously we reported that serum IL‐18 levels were elevated in the sera from atopic dermatitis‐model mice NC/Nga, prior to the onset and during the development of dermatitis. Objectives We studied whether neutralization of IL‐18 activity might affect dermatitis in NC/Nga mice, to investigate the role of IL‐18 on dermatitis. Methods NC/Nga mice were given weekly anti‐IL‐18 antibody starting at 5 weeks of age to 13 weeks and development of dermatitis, scratching behaviour and serum IgE concentrations were evaluated. Results Continuous injections of anti‐IL‐18 antibody failed to inhibit the onset and development of dermatitis and IgE elevation. The treatment, rather, tended to lead to an exacerbation of dermatitis and scratching behaviour. In addition, the administration of anti‐IL‐18 antibody did not ameliorate the responsiveness of lymphocytes to IL‐4, which was previously demonstrated as an immunological abnormality in the mouse. Conclusion This study demonstrates that, at least in NC/Nga mice, IL‐18, although excessively expressed before the onset of dermatitis, shows antiallergic actions.