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2016 ; 2016
(ä): 1719720
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The Role of TLR4 on B Cell Activation and Anti-?(2)GPI Antibody Production in the
Antiphospholipid Syndrome
#MMPMID27868072
Cheng S
; Wang H
; Zhou H
J Immunol Res
2016[]; 2016
(ä): 1719720
PMID27868072
show ga
High titer of anti-?(2)-glycoprotein I antibodies (anti-?(2)GPI Ab) plays a
pathogenic role in antiphospholipid syndrome (APS). Numerous studies have focused
on the pathological mechanism in APS; however, little attention is paid to the
immune mechanism of production of anti-?(2)GPI antibodies in APS. Our previous
study demonstrated that Toll-like receptor 4 (TLR4) plays a vital role in the
maturation of bone marrow-derived dendritic cells (BMDCs) from the mice immunized
with human ?(2)-glycoprotein I (?(2)GPI). TLR4 is required for the activation of
B cells and the production of autoantibody in mice treated with ?(2)GPI. However,
TLR4 provides a third signal for B cell activation and then promotes B cells
better receiving signals from both B cell antigen receptor (BCR) and CD40, thus
promoting B cell activation, surface molecules expression, anti-?(2)GPI Ab
production, and cytokines secretion and making B cell functioning like an antigen
presenting cell (APC). At the same time, TLR4 also promotes B cells producing
antibodies by upregulating the expression of B-cell activating factor (BAFF). In
this paper, we aim to review the functions of TLR4 in B cell immune response and
antibody production in autoimmune disease APS and try to find a new way for the
prevention and treatment of APS.