Role of OX40 signals in coordinating CD4 T cell selection, migration, and cytokine differentiation in T helper (Th)1 and Th2 cells.
Role of OX40 signals in coordinating CD4 T cell selection, migration, and cytokine differentiation in T helper (Th)1 and Th2 cells.
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DOI：
10.1084/jem.191.2.201
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发表时间：
2000-01-17
期刊：
影响因子：
--
通讯作者：
Lane P
中科院分区：
文献类型：
--
作者：
Lane P
我们的生存取决于我们克隆扩增稀有CD4淋巴细胞并指导它们帮助效应细胞的能力。保护性免疫需要两种不同类型的CD4 T细胞反应。对细胞内感染（如结核病）的免疫依赖于启动和扩大炎性IFN——表达CD4 T细胞，这些细胞获得迁移到组织中并激活巨噬细胞杀死感染细胞的能力。相比之下，对白喉产生的外毒素的免疫需要CD4 T细胞被诱导迁移到B卵泡中，以促进生发中心（GC）的发育和高亲和力中和抗体的快速产生。虽然这两种类型的CD4应答的结果不同，但它们具有相同的三个组成部分：(a)抗原特异性CD4 T细胞的识别和扩增；(b)指示分泌适当的细胞因子；(c)指示表达趋化因子和粘附分子，引导它们迁移到合适的位置。最近的证据表明，树突状细胞（dc）在启动过程中直接引导CD4 T细胞的命运(1)，这使得人们关注CD4免疫应答启动时的共刺激相互作用。除了它们通过CD28配体和IL-12共同刺激CD4细胞的潜力外，dc最近被证明（2,3）表达CD4活化抗原OX40的配体。OX40及其配体在CD4 T细胞启动过程中均上调(4)，图1显示了一个模型，说明了假定的共刺激事件。
Our survival depends on our ability to clonally expand rare CD4 lymphocytes and instruct them to help effector cells. Two very different types of CD4 T cell response are required for protective immunity. Immunity to intracellular infections like tuberculosis is dependent on priming and expanding inflammatory IFN-–expressing CD4 T cells that acquire the capability to migrate out into the tissue and activate macrophages to kill infected cells. In contrast, immunity to the exotoxin produced by diphtheria requires CD4 T cells to be primed to migrate into B follicles to foster germinal center (GC) development and the rapid production of high-affinity neutralizing antibodies. Although the outcomes of these two types of CD4 response are different, they have the same three components:(a) Identification and expansion of antigen-specific CD4 T cells;(b) instruction to secrete the appropriate cytokines; and (c) instruction to express chemokine and adhesion molecules that guide their migration to the appropriate location. Recent evidence has highlighted the fact that dendritic cells (DCs) direct CD4 T cell fate during priming (1), and this has focused attention on costimulatory interactions at the initiation of CD4 immune responses. In addition to their potential to costimulate CD4 cells through CD28 ligands and IL-12, DCs have recently been shown (2, 3) to express the ligand for the CD4 activation antigen, OX40. Both OX40 and its ligand are upregulated during CD4 T cell priming (4), and a model that illustrates the putative costimulatory events is shown in Fig. 1.
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DOI：
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发表时间：
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期刊：
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影响因子：
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期刊：
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