RECEPTOR MEDIATED T AND B CELL ACTIVATION

先前激活历史对克隆的后续反应的影响 检测辅助性T细胞1(Th1)对TCR介导的刺激的反应。Th1细胞 通过单独用IL2刺激或用IL2刺激 除IL2外，还有特异性抗原和APC。单元格携带在两个 对抗CD3抗体的反应相当于条件的增殖。 然而，抗CD3抗体可诱导强烈的磷脂酰肌醇(PI)水解和 仅刺激维持的细胞内[Ca++]i升高 IL-2单独作用；经特异性抗原+APC刺激的细胞 对PI和Ca~(++)无反应。所使用的信号通路 Th1细胞因此受到先前通过TCR刺激的影响。 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SIG交联的增殖反应 分别显著降低，尽管表达正常 大多数T和B细胞表面这些受体的水平。及早分析 这些细胞中的信号事件，[Ca~(2+)]i被测量以响应 表面受体交联化。T和B的[Ca~(2+)]_i反应 来自女佣感染的小鼠的细胞减少。B细胞对Sigg的应答 通过检测蛋白质酪氨酸进一步分析了交联物 SIG交联物诱导的磷酸化。经调查发现， 病毒感染时，有选定的酪氨酸进行性丢失 磷酸化事件与其他事件的保守性。他们的回应 因此，MAIDES小鼠B细胞的缺陷在选择的 SIG信号反应中酪氨酸磷酸化的变化。

The effect of prior activation history on subsequent responses of cloned T helper 1 (Th1) cells to TCR-mediated stimuli was examined. Th1 cells were maintained by stimulation with IL2 alone or by stimulation with specific antigen and APC in addition to IL2. Cells carried under both conditions proliferated equivalently in response to anti-CD3 antibody. However, anti-CD3 induced strong phosphatidyl inositol (PI) hydrolysis and increased [Ca++]i only in cells that had been maintained by stimulation with IL2 alone; cells that had been stimulated with specific antigen + APC gave neither PI nor Ca++ responses. The signaling pathways utilized by Th1 cells were thus influenced by prior stimulation through the TCR. 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 crosslinking were further analyzed by examining protein tyrosine phosphorylation induce 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.