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CD40配体(CD154)刺激巨噬细胞产生具有HIV-1抑制作用的β趋化因子。

CD40 ligand (CD154) stimulation of macrophages to produce HIV-1-suppressive beta-chemokines.

作者信息

Kornbluth R S, Kee K, Richman D D

机构信息

Department of Medicine, University of California, San Diego, and Department of Veterans Affairs Medical Center, La Jolla, CA 92093, USA.

出版信息

Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):5205-10. doi: 10.1073/pnas.95.9.5205.

Abstract

beta-chemokines play an important role in the development of immunologic reactions. Macrophages are major beta-chemokine-producing cells during T-cell directed, delayed-type hypersensitivity reactions in tissues, and have been reported to be important producers of beta-chemokines in the lymph nodes of HIV-1-infected individuals. However, the physiological signals responsible for inducing macrophages to produce beta-chemokines have not been established. Two soluble T cell products, interferon-gamma and granulocyte-macrophage colony stimulating factor, were added to cultured macrophages, but failed to stimulate the production of macrophage inflammatory protein-1alpha and -1beta; regulated upon activation, normal T cell expressed and secreted (RANTES); or monocyte chemoattractant protein-1. Instead, direct cell-cell contact between macrophages and cells engineered to express CD40L (also known as CD154) resulted in the production of large amounts of macrophage inflammatory protein-1alpha and -1beta, and RANTES (all ligands for CCR5), and monocyte chemoattractant protein-1 (a ligand for CCR2). Supernatants from CD40L-stimulated macrophages protected CD4(+) T cells from infection by a nonsyncytium-inducing strain of HIV-1 (which uses CCR5 as a coreceptor). These results have implications for granulomatous diseases, and conditions such as atherosclerosis and multiple sclerosis, where CD40L-bearing cells have been found in the macrophage-rich lesions where beta-chemokines are being produced. Overall, these findings define a pathway linking the specific recognition of antigen by T cells to the production of beta-chemokines by macrophages. This pathway may play a role in anti-HIV-1 immunity and the development of immunologic reactions or lesions.

摘要

β-趋化因子在免疫反应的发展中起重要作用。巨噬细胞是组织中T细胞介导的迟发型超敏反应期间产生β-趋化因子的主要细胞,并且据报道是HIV-1感染个体淋巴结中β-趋化因子的重要产生者。然而,负责诱导巨噬细胞产生β-趋化因子的生理信号尚未明确。将两种可溶性T细胞产物,即干扰素-γ和粒细胞-巨噬细胞集落刺激因子添加到培养的巨噬细胞中,但未能刺激巨噬细胞炎性蛋白-1α和-1β、活化调节正常T细胞表达和分泌因子(RANTES)或单核细胞趋化蛋白-1的产生。相反,巨噬细胞与经基因工程改造以表达CD40L(也称为CD154)的细胞之间的直接细胞间接触导致大量巨噬细胞炎性蛋白-1α和-1β、RANTES(均为CCR5的配体)以及单核细胞趋化蛋白-1(CCR2的配体)的产生。CD40L刺激的巨噬细胞的上清液可保护CD4(+) T细胞免受非融合诱导型HIV-1毒株(其使用CCR5作为共受体)的感染。这些结果对肉芽肿性疾病以及动脉粥样硬化和多发性硬化症等病症具有启示意义,在这些病症中,在产生β-趋化因子的富含巨噬细胞的病变中发现了携带CD40L的细胞。总体而言,这些发现确定了一条将T细胞对抗原的特异性识别与巨噬细胞产生β-趋化因子联系起来的途径。该途径可能在抗HIV-1免疫以及免疫反应或病变的发展中起作用。

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