RECEPTOR MEDIATED T AND B CELL ACTIVATION

分析了T和B淋巴细胞中受体介导的激活 正常小鼠和感染了女佣缺陷小鼠的小鼠 小鼠白血病病毒。病毒感染几周后， T细胞和B细胞对TCR和TCR基因交联物的增殖反应 SIG分别显著降低，尽管表达了 大多数T和B细胞表面这些受体的水平正常。至 分析这些细胞中的早期信号事件，[Ca2+]i在 对表面受体交联的反应。血管内皮细胞内钙离子的反应 女佣感染小鼠的T细胞和B细胞均下降。B细胞 通过研究，进一步分析了对Sig交联的反应 SIG交联诱导的蛋白质酪氨酸磷酸化。确实是 发现在病毒感染后，有一种进行性的损失 部分酪氨酸磷酸化事件与其他 事件。因此，来自女系小鼠的B细胞的反应缺陷 反映在酪氨酸磷酸化的选择性改变中 对SIG信号的响应。

Receptor-mediated activation was analyzed in T and B lymphocytes from normal mice and from mice infected with the MAIDS-inducing defective murine leukemia virus. Several weeks after viral infection, the proliferative responses of T and B cells to cross-linking of TCR and sIg respectively were significantly reduced despite the expression of normal surface levels of these receptors by most T and B cells. To analyze early signaling events in these cells, [Ca2+]i was measured in response to surface receptor cross-linking. The [Ca2+]i responses of both T and B cells from MAIDS-infected mice were decreased. B cell responses to sIg cross-linking were further analyzed by examining protein tyrosine phosphorylation induced by sIg cross-linking. It was found that after virus infection, there was a progressive loss of selected tyrosine phosphorylation events with conservation of other events. The response defect in B cells from MAIDS mice is thus reflected in selected alterations of tyrosine phosphorylation in response to sIg signaling.