CD39 and allergic diseases
CD39 expressed in Tregs is involved in a variety of allergic diseases. Tregs can suppress contact hypersensitivity reactions through a CD39, adenosine-dependent mechanism by blocking leukocyte adhesion to endothelium [155]. Tregs remove eATP by CD39 and, therefore, abrogate the shedding of CD62L, leading to defective sensitization in contact hypersensitivity reactions[156]. CD39 mediates the protective role of CD4+Foxp3+Tregs in allergic airway inflammation by regulating ATP and ADO levels[157]. In allergic asthma, increased Tc2 and Tc17 may be related to insufficient CD39+Tregs[158]. Wang et al. found that the plasticity of Tregs transforming into IL-17+Foxp3+CD4+T-cells, the reduced frequency of CD39+ Tregs, and the less effective suppression of IL‑17 produced by residual CD39+ Tregs leads to an imbalance of Th17 and Tregs in asthma [159]. CD39 expression was down-regulated in allergic asthma and was positively correlated with serum IL-4, IL-17A, and GATA3 expression and negatively correlated with serum TGF-β and Foxp3 expression [160]. CD39 deficient DCs exhibit limited capacity to induce Th2 immunity in a DC-driven model of allergic airway inflammation in vivo [161]. Li et al. demonstrated that a reduction in CD39 expression may be associated with the development of allergic airway inflammation and that apyrase alleviates airway inflammation by decreasing the chemotactic migration of DCs towards eATP [162].