Burst-enhancing role of the IgG membrane tail as a molecular determinant of memory
Burst-enhancing role of the IgG membrane tail as a molecular determinant of memory
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DOI：
10.1038/ni752
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发表时间：
2002-02-01
影响因子：
30.5
通讯作者：
Goodnow, CC
中科院分区：
文献类型：
--
作者：
Martin, SW;Goodnow, CC
免疫记忆导致二次抗体反应增强的基础是一个长期悬而未决的问题。在这里，我们表明，一个单一的不可逆的分子变化，在B细胞抗原受体，这是由免疫球蛋白M（IgM）IgG同种型转换所带来的，是足以大大增加滤泡外增殖爆发的抗原特异性B细胞。IgG独特的跨膜区域不改变体内抗原特异性B细胞的T细胞依赖性活化和增殖，但显著增加子代细胞和浆母细胞的数量。这些结果建立了免疫记忆的关键分子决定因素，并定义了一个意想不到的细胞基础，通过它增强了二级抗体应答的幅度。
The basis of immune memory leading to heightened secondary antibody responses is a longstanding unanswered issue. Here we show that a single irreversible molecular change in the B cell antigen receptor, which is brought about by immunoglobulin M (IgM) to IgG isotype switching, is sufficient to greatly increase the extrafollicular proliferative burst of antigen-specific B cells. The unique membrane-spanning regions of IgG do not alter the T cell-dependent activation and proliferation of antigen-specific B cells in vivo, but markedly increase the number of progeny cells and plasmablasts that accumulate. These results establish a key molecular determinant of immunological memory and define an unexpected cellular basis by which it enhances the magnitude of secondary antibody responses.