An autoimmune disease variant of IgG1 modulates B cell activation and differentiation
文献类型:期刊论文
作者 | Chen, Xiangjun1; Yang, Bing1; Chen, Shuting1; He, Lili1; Yang, Changmei1; Xiao, Le1; Liu, Wanli1,17; Sun, Xiaolin2; Zhao, Xiaozhen2; Guo, Jianping2 |
刊名 | SCIENCE |
出版日期 | 2018 |
卷号 | 362期号:6415页码:700-+ |
ISSN号 | 0036-8075 |
关键词 | Systemic-lupus-erythematosus Autoantibody Production Plasma-cells Memory Tail Roles Mice |
DOI | 10.1126/science.aap9310 |
文献子类 | Article |
英文摘要 | The maintenance of autoreactive B cells in a quiescent state is crucial for preventing autoimmunity. Here we identify a variant of human immunoglobulin G1 (IgG1) with a Gly(396)-> Arg substitution (hIgG1-G396R), which positively correlates with systemic lupus erythematosus. In induced lupus models, murine homolog Gly(390)-> Arg (G390R) knockin mice generate excessive numbers of plasma cells, leading to a burst of broad-spectrum autoantibodies. This enhanced production of antibodies is also observed in hapten-immunized G390R mice, as well as in influenza-vaccinated human G396R homozygous carriers. This variant potentiates the phosphorylation of the IgG1 immunoglobulin tail tyrosine (ITT) motif. This, in turn, alters the availability of phospho-ITT to trigger longer adaptor protein Grb2 dwell times in immunological synapses, leading to hyper-Grb2- Bruton's tyrosine kinase (Btk) signaling upon antigen binding. Thus, the hIgG1-G396R variant is important for both lupus pathogenesis and antibody responses after vaccination. |
电子版国际标准刊号 | 1095-9203 |
WOS研究方向 | Multidisciplinary Sciences |
语种 | 英语 |
WOS记录号 | WOS:000450474500044 |
版本 | 出版稿 |
源URL | [http://202.127.25.143/handle/331003/3378] |
专题 | 生化所2018年发文 |
通讯作者 | Liu, Wanli; Li, Zhanguo |
作者单位 | 1.Tsinghua Univ, Collaborat Innovat Ctr Diag & Treatment Infect Di, Key Lab Prot Sci, Minist Educ,Ctr Life Sci,Inst Immunol,Sch Life Sc, Beijing 100084, Peoples R China; 2.Peking Univ, Beijing Key Lab Rheumatism & Immune Diag BZ0135, State Key Lab Nat & Biomimet Drugs, Dept Rheumatol & Immunol,Peoples Hosp,Peking Tsin, Beijing 100044, Peoples R China; 3.Tsinghua Univ, Sch Life Sci, Beijing 100084, Peoples R China; 4.Chinese Acad Sci, Inst Biophys, Lab RNA Biol, Beijing 100101, Peoples R China; 5.Chinese Acad Sci, Key Lab Pathogen Microbiol & Immunol, Inst Microbiol, Beijing 100101, Peoples R China; 6.Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Basic Med, Dept Immunol, Wuhan 430030, Hubei, Peoples R China; 7.Nanjing Med Univ, Sch Publ Hlth, Ctr Global Hlth, Dept Epidemiol, Nanjing 211166, Jiangsu, Peoples R China; 8.Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA; 9.Peking Union Med Coll, Peking Union Med Coll Hosp, Dept Rheumatol & Clin Immunol, Beijing 100730, Peoples R China; 10.Chinese Acad Med Sci, Beijing 100730, Peoples R China; |
推荐引用方式 GB/T 7714 | Chen, Xiangjun,Yang, Bing,Chen, Shuting,et al. An autoimmune disease variant of IgG1 modulates B cell activation and differentiation[J]. SCIENCE,2018,362(6415):700-+. |
APA | Chen, Xiangjun.,Yang, Bing.,Chen, Shuting.,He, Lili.,Yang, Changmei.,...&Lai, Luhua.(2018).An autoimmune disease variant of IgG1 modulates B cell activation and differentiation.SCIENCE,362(6415),700-+. |
MLA | Chen, Xiangjun,et al."An autoimmune disease variant of IgG1 modulates B cell activation and differentiation".SCIENCE 362.6415(2018):700-+. |
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