title: The Role of TLR4 on B Cell Activation and Anti-β2GPI Antibody Production in the Antiphospholipid Syndrome.
abstract: High titer of anti-β2-glycoprotein I antibodies (anti-β2GPI 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-β2GPI 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 humanβ2-glycoprotein I (β2GPI). TLR4 is required for the activation of B cells and the production of autoantibody in mice treated withβ2GPI. 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-β2GPI 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.
authors.affiliation: Department of Pediatrics, The Affiliated People's Hospital, Jiangsu University, Zhenjiang, Jiangsu 212002, China; Department of Laboratory Medicine, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China; Department of Clinical Laboratory and Hematology, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, China.
authors.forename: Si
authors.identifier: 0000-0002-8683-510X
authors.initials: S
authors.lastname: Cheng
authors.affiliation: Department of Pediatrics, The Affiliated People's Hospital, Jiangsu University, Zhenjiang, Jiangsu 212002, China.
authors.forename: Haibo
authors.identifier: 0000-0001-7575-9474
authors.initials: H
authors.lastname: Wang
authors.affiliation: Department of Clinical Laboratory and Hematology, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, China.
authors.forename: Hong
authors.identifier: 0000-0003-1825-0342
authors.initials: H
authors.lastname: Zhou
mesh_terms: D000818:Animals; D017152:Antibodies, Antiphospholipid / Q000096:biosynthesis / Q000276:immunology*; D000917:Antibody Formation / Q000276:immunology*; D016736:Antiphospholipid Syndrome / Q000276:immunology* / Q000378:metabolism* / Q000628:therapy; D001324:Autoantigens / Q000276:immunology; D015551:Autoimmunity; D053264:B-Cell Activating Factor / Q000378:metabolism; D001402:B-Lymphocytes / Q000276:immunology* / Q000378:metabolism*; D002454:Cell Differentiation / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007167:Immunotherapy; D008213:Lymphocyte Activation / Q000276:immunology*; D058990:Molecular Targeted Therapy; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000378:metabolism*; D053482:beta 2-Glycoprotein I / Q000276:immunology
chemical_list: D017152:Antibodies, Antiphospholipid; D001324:Autoantigens; D053264:B-Cell Activating Factor; D016207:Cytokines; D051197:Toll-Like Receptor 4; D053482:beta 2-Glycoprotein I