The role of human T-lymphocyte-monocyte contact in inflammation and tissue destruction.

The role of human T-lymphocyte-monocyte contact in inflammation and tissue destruction.
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DOI:
10.1186/ar558
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发表时间:
2002
期刊:
Arthritis research
影响因子:
--
通讯作者:
Dayer JM
Dayer JM
中科院分区:
其他
文献类型:
--
作者:
Burger D;Dayer JM

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人刺激T淋巴细胞(TL)接触介导的单核细胞信号传导是一种有效的促炎机制,可触发促炎细胞因子IL-1和肿瘤坏死因子-α的大量上调。这两种细胞因子在包括类风湿性关节炎在内的慢性破坏性疾病中发挥重要作用。迄今为止,这种细胞-细胞接触似乎是单核细胞-巨噬细胞中显示这种活性的主要内源性机制。由于TL和单核-巨噬细胞在慢性炎症性疾病的发病机制中起关键作用,我们研究了参与这种细胞-细胞相互作用的可能的配体和反配体。我们还表征了干扰这一过程的抑制性分子,载脂蛋白A-I。本文综述了类风湿关节炎中接触介导的单核细胞活化的重要性及其调控机制。
Contact-mediated signaling of monocytes by human stimulated T lymphocytes (TL) is a potent proinflammatory mechanism that triggers massive upregulation of the proinflammatory cytokines IL-1 and tumor necrosis factor-α. These two cytokines play an important part in chronic destructive diseases, including rheumatoid arthritis. To date this cell–cell contact appears to be a major endogenous mechanism to display such an activity in monocyte-macrophages. Since TL and monocyte-macrophages play a pivotal part in the pathogenesis of chronic inflammatory diseases, we investigated the possible ligands and counter-ligands involved in this cell–cell interaction. We also characterized an inhibitory molecule interfering in this process, apolipoprotein A-I. This review aims to summarize the state of the art and importance of contact-mediated monocyte activation by stimulated TL in cytokine production in rheumatoid arthritis and mechanisms that might control it.
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