Impaired T cell-mediated macrophage activation in CD40 ligand-deficient mice.
Impaired T cell-mediated macrophage activation in CD40 ligand-deficient mice.
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DOI：
10.4049/jimmunol.156.1.8
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发表时间：
1996-01
影响因子：
4.4
通讯作者：
R. Stout;J. Suttles;Jianchao Xu;I. Grewal;R. Flavell
中科院分区：
文献类型：
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作者：
R. Stout;J. Suttles;Jianchao Xu;I. Grewal;R. Flavell
CD40配体(CD40L)的表达是诱导T细胞依赖的抗体应答的关键。为了检测CD40L的表达对诱导细胞免疫反应的关键作用，我们评估了CD40L基因敲除小鼠的T细胞激活巨噬细胞效应功能的能力。来自CD40L基因敲除小鼠的CD4+T细胞在激活同种异体巨噬细胞中的一氧化氮反应方面的效率比+/+T细胞低四倍。CD40L基因敲除的T细胞在6小时的激活期后用多聚甲醛固定，CD40L在T细胞的巨噬细胞激活能力中占据主导地位，既不能激活巨噬细胞产生炎性细胞因子(TNF-α)，也不能产生活性氮中间产物。然而，激活24小时后，CD40L基因敲除的T细胞和+/+T细胞均可诱导类似但微弱的巨噬细胞反应。这项研究表明，CD40L表达缺陷的动物在T细胞依赖的巨噬细胞介导的免疫反应方面存在缺陷。
The expression of the ligand for CD40 (CD40L) is critical for induction of T cell-dependent Ab responses. To examine how critical the expression of CD40L is for induction of cell-mediated immune responses, the ability of T cells from CD40L knockout mice to activate macrophage effector function was assessed. CD4+ T cells from CD40L-knockout mice were fourfold less effective than +/+ T cells in activating the nitric oxide response in allogeneic macrophages. CD40L-knockout T cells that were fixed with paraformaldehyde after a 6-h activation period, a time point at which CD40L dominates the macrophage-activating capability of the T cell, could activate neither macrophage production of inflammatory cytokines (TNF-alpha) nor generation of reactive nitrogen intermediates. After 24 h of activation, however, both CD40L-knockout and +/+ T cells could induce similar but weak responses from the macrophages. This study demonstrates that animals deficient in CD40L expression display a deficiency in T cell-dependent macrophage-mediated immune responses.