Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells

Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells
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DOI:
10.1126/science.1132742
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发表时间:
2006-11-17
期刊:
影响因子:
56.9
通讯作者:
von Andrian, Ulrich H.
von Andrian, Ulrich H.
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Mora, J. Rodrigo;Iwata, Makoto;von Andrian, Ulrich H.

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正常肠粘膜含有丰富的免疫球蛋白A(IgA)分泌细胞,这些细胞由肠道相关淋巴组织(GALT)中的B细胞产生。我们发现来自GALT的树突状细胞(DC)诱导B细胞上非T细胞依赖性的IgA和肠归巢受体的表达。GALT-DC衍生的维甲酸(RA)单独具有胃肠功能,但不能促进IgA的分泌。然而,RA与GALT-DC来源的IL-6或IL-5有很强的协同作用,诱导IgA分泌。因此,缺乏RA前体维生素A的小鼠在小肠中缺乏分泌IgA的细胞。因此,GalT-DC通过协同作用的介质调节B细胞的迁移和效应器的活性,从而形成粘膜免疫。
Normal intestinal mucosa contains abundant immunoglobulin A (IgA) - secreting cells, which are generated from B cells in gut-associated lymphoid tissues (GALT). We show that dendritic cells ( DC) from GALT induce T cell - independent expression of IgA and gut-homing receptors on B cells. GALT-DC-derived retinoic acid (RA) alone conferred gut tropism but could not promote IgA secretion. However, RA potently synergized with GALT-DC-derived interleukin-6 (IL-6) or IL-5 to induce IgA secretion. Consequently, mice deficient in the RA precursor vitamin A lacked IgA-secreting cells in the small intestine. Thus, GALT-DC shape mucosal immunity by modulating B cell migration and effector activity through synergistically acting mediators.