T CELL FUNCTION IN T CELL DEPLETED STATES

产生T细胞群体的机制与 T细胞免疫重建的思考 耗尽就会发生。恒河猴T细胞的研究 T细胞耗尽的自体骨髓移植后的一代 提供了输注的T细胞中残留的T细胞耗尽的证据 骨髓在后续T细胞的产生中起核心作用 人口。这种可能性在#年的小鼠研究中得到证实。 确定了哪三个T细胞祖细胞池对 最终达到骨髓移植后T细胞的再分化。确实是 发现细胞起源于外周成熟的淋巴细胞 前体库具有记忆表型，且只有T细胞 由胸腺途径产生的含有大量幼稚T细胞 细胞。这些信息已被应用于T细胞的研究 在接受化疗的患者中表现出年龄的一代 依赖于胸腺产生T细胞&提供了一种 T细胞生成可在其他领域研究的范例 情况。再生T细胞的功能特性 人口也是令人感兴趣的。人类辅助性T细胞对 异种MHC编码抗原刺激小鼠细胞表达 对种群进行了研究，发现它们在 人类辅助性T细胞功能的评估 响应需要对刺激的小鼠抗原进行再处理 与人类II类基因产物相关的展示。这个 小鼠抗原再加工的要求及呈递 发现了反应型细胞(而不是小鼠刺激细胞) 这是由于缺乏小鼠抗原提呈细胞的激活和 应答者人类T细胞激活。此外，GM-CSF提供了一种 给小鼠APC足够的信号导致B7-2上调， 使小鼠抗原提呈细胞能够直接提呈抗原 人类辅助性T细胞。

Mechanisms by which T cell populations are generated are relevant to considerations of immunoreconstitution in situations in which T cell depletion occurs. Studies in rhesus monkeys investigating T cell generation following T cell depleted autologous marrow transplantation provided evidence that residual T cells in infused T cell-depleted marrow play a central role in the generation of subsequent T cell populations. This possibility was confirmed in murine studies in which three T cell progenitor pools were identified which contribute to final T cell repopulation following marrow transplantation. It was found that cells arising from a peripheral, mature lymphocyte precursor pool were of memory phenotype, and that only T cells generated by a thymic pathway contained large numbers of naive T cells. This information has been applied to studies of T cell generation in patients receiving chemotherapy which have shown an age dependence on generation of T cells by the thymus & have provided a paradigm by which T cell generation might be studied in other circumstances. The functional capacities of regenerated T cell populations is also of interest. The human T helper cell response to xenogeneic MHC encoded antigens expressed by stimulating murine cell populations has been studied & found to be of special use in the assessment of human T helper cell function in that this primary response requires reprocessing of the stimulating murine antigens & presentation in association with human Class II gene products. The requirement for reprocessing of murine antigen & presentation by responder-type cells (rather than murine stimulating cells) was found to be due to lack of both murine antigen presenting cell activation & responder human T cell activation. Further, GM-CSF provided a sufficient signal to murine APC to result in upregulation of B7-2, enabling murine antigen presenting cells to directly present antigen to human T helper cells.