The Role of TLR4 on B Cell Activation and Anti-β(2)GPI Antibody Production in the Antiphospholipid Syndrome.
The Role of TLR4 on B Cell Activation and Anti-β(2)GPI Antibody Production in the Antiphospholipid Syndrome.
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TLR4 在抗磷脂综合征中 B 细胞激活和抗 β(2)GPI 抗体产生中的作用
DOI：
10.1155/2016/1719720
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发表时间：
2016
影响因子：
4.1
通讯作者：
Zhou H
中科院分区：
文献类型：
--
作者：
Cheng S;Wang H;Zhou H
高滴度抗β2-糖蛋白I抗体(抗β2GPI Ab)在抗磷脂综合征(APS)中起致病作用。许多研究都集中在AP的发病机制上，而抗β2GPI抗体在AP中产生的免疫机制却鲜有人关注。我们先前的研究表明，Toll样受体4(TLR4)在人β2-糖蛋白I(β2GPI)免疫的小鼠骨髓来源的树突状细胞(BMDCs)成熟过程中起着至关重要的作用。在β2GPI处理的小鼠中，TLR4是激活B细胞和产生自身抗体所必需的。而TLR4为B细胞的激活提供第三种信号，进而促进B细胞更好地接受B细胞抗原受体和CD40的信号，从而促进B细胞活化、表面分子表达、抗β2GPI抗体的产生和细胞因子的分泌，使B细胞发挥抗原提呈细胞的功能。同时，TLR4还通过上调B细胞激活因子(BAFF)的表达促进B细胞产生抗体。本文就TLR4在自身免疫性疾病APS的B细胞免疫应答和抗体产生中的作用作一综述，以期为APS的防治寻找新的途径。
High titer of anti-β 2-glycoprotein I antibodies (anti-β 2GPI 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-β 2GPI 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 β 2-glycoprotein I (β 2GPI). TLR4 is required for the activation of B cells and the production of autoantibody in mice treated with β 2GPI. 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-β 2GPI 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.
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影响因子：
3.7
作者：
Boeglin E;Smulski CR;Brun S;Milosevic S;Schneider P;Fournel S
通讯作者：
Fournel S
影响因子：
3
作者：
Bornacelly A;Mercado D;Acevedo N;Caraballo L
通讯作者：
Caraballo L
影响因子：
20.3
作者：
Colasanti, Tania;Alessandri, Cristiano;Margutti, Paola
通讯作者：
Margutti, Paola
DOI：
10.4049/jimmunol.0901689
发表时间：
2010-07-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Bolduc A;Long E;Stapler D;Cascalho M;Tsubata T;Koni PA;Shimoda M
通讯作者：
Shimoda M
影响因子：
3
作者：
Dasu MR;Jialal I
通讯作者：
Jialal I