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].