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10.1155/2016/1719720

http://scihub22266oqcxt.onion/10.1155/2016/1719720
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C5102736!5102736 !27868072
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suck abstract from ncbi


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pmid27868072
      J+Immunol+Res 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.
  • |Animals [MESH]
  • |Antibodies, Antiphospholipid/biosynthesis/*immunology [MESH]
  • |Antibody Formation/*immunology [MESH]
  • |Antiphospholipid Syndrome/*immunology/*metabolism/therapy [MESH]
  • |Autoantigens/immunology [MESH]
  • |Autoimmunity [MESH]
  • |B-Cell Activating Factor/metabolism [MESH]
  • |B-Lymphocytes/*immunology/*metabolism [MESH]
  • |Cell Differentiation/immunology [MESH]
  • |Cytokines/metabolism [MESH]
  • |Humans [MESH]
  • |Immunotherapy [MESH]
  • |Lymphocyte Activation/*immunology [MESH]
  • |Molecular Targeted Therapy [MESH]
  • |Signal Transduction [MESH]
  • |T-Lymphocytes/immunology/metabolism [MESH]
  • |Toll-Like Receptor 4/*metabolism [MESH]


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