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The role of TLR 4 in pathophysiology of antiphospholipid syndrome‐associated thrombosis and pregnancy morbidity
Author(s) -
Xie Hongxiang,
Sheng Liangju,
Zhou Hong,
Yan Jinchuan
Publication year - 2014
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/bjh.12587
Subject(s) - antiphospholipid syndrome , signal transduction , immunology , microbiology and biotechnology , annexin a5 , receptor , biology , annexin a2 , medicine , cancer research , antibody , annexin , flow cytometry
Summary The antiphospholipid syndrome ( APS ) is an autoimmune disease characterized by the clinical features of recurrent thrombosis in the venous or arterial circulation and fetal losses. Antiphospholipid antibodies ( aPL ), particularly against the phospholipid binding protein beta‐2 glycoprotein I (β2 GPI ), play an important role in APS pathological mechanisms. aPL can activate intracellular signal transduction in a β2 GPI ‐dependent manner to induce inflammatory responses, and promote hypercoagulable state and recurrent spontaneous abortion when β2 GPI is associated with the cell surface receptor. In vivo and in vitro studies show that Annexin A 2 ( ANXA 2) is the high affinity receptor that connects β2 GPI to the target cells. However, ANXA 2 is not a transmembrane protein and lacks an intracellular signal transduction pathway. Growing evidences suggest that the transmembrane protein toll‐like receptor 4 ( TLR 4) might act as an ‘adaptor’ for intracellular signal transduction. This review focuses on the role of TLR 4 and its signalling pathway in APS pathological mechanisms which will help us better understand the pathological processes of this syndrome.