Immune regulation by the ST6Gal sialyltransferase
Immune regulation by the ST6Gal sialyltransferase
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DOI：
10.1073/pnas.95.8.4504
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发表时间：
1998-04-14
影响因子：
11.1
通讯作者：
Marth, JD
中科院分区：
文献类型：
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作者：
Hennet, T;Chui, D;Marth, JD
ST 6 Gal唾液酸转移酶控制Sia α 2- 6 Gal β 1-4GlcNAc（Sia 6LacNAc）三糖的产生，其是凝集素CD 22的配体。CD 22与Sia 6 GlacNAc的结合涉及调节淋巴细胞粘附和活化。我们研究了缺乏ST 6 Gal的小鼠，并报告它们是可行的，但表现出严重的免疫抑制的标志，不像CD 22缺陷小鼠。值得注意的是，Sia 6 LacNAc缺陷型小鼠显示血清IgM水平降低，响应IgM和CD 40交联的B细胞增殖受损，以及针对T非依赖性和T依赖性抗原的抗体产生减弱。进一步发现ST 6 Gal的缺乏改变了从B淋巴细胞抗原受体的信号转导期间磷酸酪氨酸的积累。这些研究表明，ST 6 Gal唾液酸转移酶和相应的Sia 6 LacNAc寡糖的产生在促进B淋巴细胞活化和免疫功能中是必需的。
The ST6Gal sialyltransferase controls production of the Sia alpha 2-6Gal beta 1-4GlcNAc (Sia6LacNAc) trisaccharide, which is the ligand for the lectin CD22. Binding of CD22 to Sia6GLacNAc is implicated in regulating lymphocyte adhesion and activation. We have investigated mice that lack ST6Gal and report that they are viable, yet exhibit hallmarks of severe immunosuppression unlike CD22-deficient mice. Notably, Sia6LacNAc-deficient mice display reduced serum IgM levels, impaired B cell proliferation in response to IgM and CD40 crosslinking, and attenuated antibody production to T-independent and T-dependent antigens. Deficiency of ST6Gal was further found to alter phosphotyrosine accumulation during signal transduction from the B lymphocyte antigen receptor. These studies reveal that the ST6Gal sialyltransferase and corresponding production of the Sia6LacNAc oligosaccharide are essential in promoting B lymphocyte activation and immune function.