Premium
CD14 + cell–derived IL‐29 modulates proinflammatory cytokine production in patients with allergic airway inflammation
Author(s) -
He S.,
Li T.,
Chen H.,
Ma W.,
Yao Q.,
Yang H.,
Wang H.,
Wang F.,
Zhao C.,
Yang P.
Publication year - 2011
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.2010.02455.x
Subject(s) - cd14 , immunology , immune system , proinflammatory cytokine , cytokine , medicine , allergic inflammation , inflammation , tumor necrosis factor alpha , t cell , allergy , interleukin , interleukin 10
To cite this article: He S, Li T, Chen H, Ma W, Yao Q, Yang H, Wang H, Wang F, Zhao C, Yang P. CD14 + cell–derived IL‐29 modulates proinflammatory cytokine production in patients with allergic airway inflammation. Allergy 2011; 66 : 238–246. Abstract Background: Interleukin (IL)‐29 is a newly described cytokine that has anti‐viral activity, induces tumor cell death and regulates immune function. Whether it plays a role in immune disorders is unclear. This study aims to examine the role of IL‐29 in the modulation of immune response under allergic environment. Methods: A group of patients with allergic asthma or/and allergic rhinitis was recruited to this study. Serum samples were collected from the patients in both in‐season and out‐season; the serum levels of IL‐29 were determined by enzyme‐linked immunoassay. Cell types of IL‐29‐producing cells in upper airway mucosa were identified with immune staining and examined by immunohistochemistry and flow cytometry. Results: High serum levels of IL‐29 were detected in patients with allergic asthma in in‐season, but not in out‐season. The majority of IL‐29 + cells in upper airway tissue were CD14 + cells. Exposure to specific antigens triggered the release of IL‐4 from antigen‐specific CD4 + T cells; the released IL‐4 activated CD14 + cells to release IL‐29; the released IL‐29 further triggered the release of IL‐6 and tumor necrosis factor from CD4 + T cells. Conclusions: Interleukin‐29 is involved in the pathogenesis of allergic inflammation via modulating immune cells’ function to release proinflammatory cytokines.