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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Masking of CD22 by cis ligands does not prevent redistribution of CD22 to sites of cell contact
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Masking of CD22 by cis ligands does not prevent redistribution of CD22 to sites of cell contact

机译：CD22被顺式配体掩盖不能阻止CD22重新分布到细胞接触部位

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摘要

CD22, a negative regulator of B cell signaling, is a member of the siglec family that binds to alpha2-6-linked sialic acids on glycoproteins. Previous reports demonstrated that binding of multivalent sialoside probes to CD22 is blocked, or "masked," by endogenous (cis) ligands, unless they are first destroyed by sialidase treatment. These results suggest that cis ligands on B cells make CD22 functionally unavailable for binding to ligands in trans. Through immunofluorescence microscopy, however, we observed that CD22 on resting B cells redistributes to the site of contact with other B or T lymphocytes. Redistribution is mediated by interaction with trans ligands on the opposing cell because it does not occur with ligand-deficient lymphocytes from ST6Gall-null mice. Surprisingly, CD45, proposed as both a cis and trans ligand of CD22, was not required for redistribution to sites of cell contact, given that redistribution of CD22 was independent of CD45 and was observed with lymphocytes from CD45-deficient mice. Furthermore, CD45 is not required for CD22 masking as similar levels of masking were observed in the WT and null mice. Comparison of the widely used sialoside-polyacrylamide probe with a sialoside-streptavidin probe revealed that the latter bound a subset of B cells without sialidase treatment, suggesting that cis ligands differentially impacted the binding of these two probes in trans. The combined results suggest that equilibrium binding to cis ligands does not preclude binding of CD22 to ligands in trans, and allows for its redistribution to sites of contact between lymphocytes.
机译：CD22是B细胞信号转导的负调节剂，是siglec家族的成员，该家族与糖蛋白上的α2-6连接的唾液酸结合。先前的报道表明，除非内含性（顺式）配体首先阻断多价唾液酸探针与CD22的结合，否则它们将被内源性（顺式）配体阻断或“掩盖”，除非它们首先被唾液酸酶处理破坏。这些结果表明，B细胞上的顺式配体使CD22在功能上不可用于反式结合配体。然而，通过免疫荧光显微镜，我们观察到静止B细胞上的CD22重新分布到与其他B或T淋巴细胞接触的部位。重新分布是通过与相对细胞上的反式配体相互作用来介导的，因为它不会发生在来自ST6Gall-null小鼠的配体缺陷型淋巴细胞中。出人意料的是，被建议作为CD22的顺式和反式配体的CD45不需要重新分布到细胞接触部位，因为CD22的重新分布不依赖于CD45，并且可以用CD45缺陷小鼠的淋巴细胞观察到。此外，CD22掩盖不需要CD45，因为在WT和空小鼠中观察到相似的掩盖水平。广泛使用的唾液酸-聚丙烯酰胺探针与唾液酸-链霉亲和素探针的比较显示，后者在未经唾液酸酶处理的情况下结合了B细胞的一部分，这表明顺式配体差异地影响了这两种探针的反式结合。组合结果表明，与顺式配体的平衡结合并不排除CD22与反式配体的结合，并允许其重新分布至淋巴细胞之间的接触位点。

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