چکیده (انگلیسی):

Allergic disorders commonly involve both chronic tissue inflammation and remodeling caused by
immunological reactions to various antigens on tissue surfaces. Due to their anatomical location, vascular
endothelial cells are the final responders to interact with various exogenous factors that come into
contact with the epithelial surface, such as pathogen-associated molecular patterns (PAMPs) and antigens.
Recent studies have shed light on the important roles of endothelial cells in the development and
exacerbation of allergic disorders. For instance, endothelial cells have the greatest potential to produce
several key molecules that are deeply involved in allergic inflammation, such as periostin and thymus
and activation-regulated chemokine (TARC/CCL17). Additionally, endothelial cells were recently shown to
be important functional targets for IL-33dan essential regulator of allergic inflammation. Notably,
almost all endothelial cell responses and functions involved in allergic inflammation are not suppressed
by corticosteroids. These corticosteroid-refractory endothelial cell responses and functions include TNFa-
associated angiogenesis, leukocyte adhesion, IL-33-mediated responses and periostin and TARC production.
Therefore, these unique responses and functions of endothelial cells may be critically involved in
the pathogenesis of various allergic disorders, especially their refractory processes. Here, we review
recent studies, including ours, which have elucidated previously unknown pathophysiological roles of
vascular endothelial cells in allergic inflammation and discuss the possibility of endothelium-targeted
therapy for allergic disorders.