Cigarette smoke (CS) facilitates adverse effects on the airway inflammation and treatment of
asthma. Here, we investigated the mechanisms by which CS exacerbates asthma. The roles …

It has been recently reported that cigarette smoke exposure during allergen sensitization
facilitates the development of allergic asthma; however, the underlying mechanisms remain …

Background Interleukin-33 (IL-33) activates group 2 innate lymphoid cells (ILC2), resulting in
T-helper-2 inflammation in bronchial asthma. Airway epithelial cells were reported as …

Previous studies have shown that IL-22, one of the Th17 cell–related cytokines, plays
multiple roles in regulating allergic airway inflammation caused by antigen-specific Th2 …

Methods ST2 deficient and Balb/c control mice were exposed nine times over a 3-week
period to house dust mite (HDM)±DEP. Seven weeks later, some mice received a single …

Abstract Interleukin 33 (IL-33) represents a potential link between the airway epithelium and
induction of Th2-type inflammatory responses associated with the development of asthma …

In several clinical and experimental studies IL-33 and its receptor have been found to play
important roles in the development of asthma and allergic airway inflammation. We …

Interleukin-33 (IL-33) and its receptor ST2 have been influentially associated with the
pathophysiology of asthma. Due to the divergent roles of IL-33 in regulating mast cell …

Neutrophilic airway inflammation is a hallmark of patients with severe asthma. Although we
have reported that both IL-33 and IL-17A contributed to IgE-mediated neutrophilic …

Alternatively activated macrophages (AAM) play a crucial role in type 2 immunity. Mice
deficient in ST2, a receptor for the latest member of the IL-1 family, IL-33, have impaired type …