Affiliation:
1. Department of Otorhinolaryngology, Nagoya City University, Nagoya, Japan This study is supported by Grant-in-Aid from the Japan Society for the Promotion of Science M. Suzuki has received Grant-in-Aid from the Japan Society for the Promotion of Science.
Abstract
Background Interleukin (IL) 35 was recently identified as an additional anti-inflammatory and immunosuppressive cytokine. However, the role of IL-35 in allergic rhinitis is not well understood. The effect of IL-35 on other cytokines in allergic responses is also unclear. Objective To investigate, in mice with allergic rhinitis, the effect of IL-35 on other cytokines associated with allergic rhinitis. Methods A murine model of allergic rhinitis was established, and splenic cells were collected. Ovalbumin-specific allergic T-cell response was measured. The production of cytokines (T helper 1 interferon-gamma), Th2 (IL-4, IL-5, IL-13), Th17 (IL-17), IL-12 family (IL-12, IL-23, IL-27), IL-2, tumor necrosis factor-alpha, transforming growth factor-beta, and IL-10) stimulated with antigen was also measured in the presence or absence of IL-35. Results IL-35 significantly inhibited the ovalbumin-specific T-cell response. It also significantly reduced the production of IL-4, IL-5, IL-13, IL-17, IL-23, and TNF-alpha, and significantly increased the production of IL-2, IL-10, and IL-27. Conclusion This study showed that IL-35 inhibits allergic T-cell response and has the ability to modulate the production of IL-2, IL-4, IL-5, IL-10, IL-13, IL-17, IL-23, IL-27, and TNF-alpha in mice with allergic rhinitis. This study also indicated the possibility of a novel therapy with IL-35 for the control of allergic rhinitis.
Subject
General Medicine,Otorhinolaryngology,Immunology and Allergy
Cited by
24 articles.
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