Pathogenesis of thromboangiitis obliterans: Gene polymorphism and immunoregulation of human vascular endothelial cells

Thromboangiitis obliterans (TAO) is a nonatherosclerotic, segmental, inflammatory vasculitis, which commonly affects the small- and medium-sized arteries of the upper and lower extremities. Despite its discovery more than a century ago, little progress has been made in its treatment. Unless the path...

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Bibliographic Details
Published in:Atherosclerosis 2017-10, Vol.265, p.258-265
Main Authors: Sun, Xiao-lei, Law, Betty Yuen-Kwan, de Seabra Rodrigues Dias, Ivo Ricardo, Mok, Simon Wing Fai, He, Yan-zheng, Wong, Vincent Kam-Wai
Format: Article
Language:English
Subjects:
Buerger's disease
Endothelial Cells - immunology
Humans
IL-33
MyD88
Polymorphism
Polymorphism, Genetic
Risk Factors
Thromboangiitis obliterans
Thromboangiitis Obliterans - genetics
Thromboangiitis Obliterans - immunology
Type 2 helper T cells
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Summary:Thromboangiitis obliterans (TAO) is a nonatherosclerotic, segmental, inflammatory vasculitis, which commonly affects the small- and medium-sized arteries of the upper and lower extremities. Despite its discovery more than a century ago, little progress has been made in its treatment. Unless the pathogenesis is elucidated, therapeutic approaches will be limited. The purpose of this review article is to collate current knowledge of mechanisms for the pathogenesis of thromboangiitis obliterans and to propose potential mechanisms from a genetic and immunoreactive point of view for its inception. Therefore, we discuss the possibility that the pathogenesis of this disease is due to a type of gene polymorphism, which leads to an immunological inflammatory vasculitis associated with tobacco abuse, highly linked to T cells, human vascular endothelial cells (HVECs), and the TLR-MyD88-NFκB pathway, distinct from arteriosclerosis obliterans and other vasculitides. •T-cell immunity and SNP of MyD88, a key regulator of TLR pathway in innate immunity, are implicated in pathogenesis of TAO.•Smoking, a major risk factor of TAO pathogenesis, would elevate IL-33 level in TAO susceptible population.•IL-33 binds to ST2 receptor on circulatory Th2 cells to activate TLR signaling and Th2 infiltration, thereby initiates TAO.
ISSN:0021-9150
1879-1484
DOI:10.1016/j.atherosclerosis.2017.08.009