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首页> 外文期刊>Journal of immunotherapy >alpha1-Adrenergic Receptor Antagonists Induce Production of IL-18 and Expression of ICAM-1 and CD40 in Human Monocytes.
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alpha1-Adrenergic Receptor Antagonists Induce Production of IL-18 and Expression of ICAM-1 and CD40 in Human Monocytes.

机译：alpha1-肾上腺素能受体拮抗剂诱导人单核细胞中IL-18的产生以及ICAM-1和CD40的表达。

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The activation of T cells plays a role in antitumor response. Monocytes activate T cells by inducing the cell-to-cell interaction that involves the engagement of adhesion molecules with their ligands, and the production of IL-18. The authors examined the effect of the quinazoline-based alpha1-adrenergic receptor antagonists bunazosin, doxazosin, prazosin, and terazosin on the expression of adhesion molecules such as ICAM-1, B7.1, B7.2, CD40, and CD40L on monocytes isolated from human peripheral blood mononuclear cells. Doxazosin, prazosin, and terazosin induced the expression of ICAM-1 and CD40 but had no effect on the expression of B7.1, B7.2, and CD40L. Moreover, IL-18 was detected in the medium of incubated monocytes treated with doxazosin, prazosin, and terazosin. Bunazosin did not affect adhesion molecule expression and IL-18 production, suggesting that the chemical structure of quinazoline might not be related to the effect of doxazosin, prazosin, and terazosin. Although caspase-1 inhibitor completely abolished the production of IL-18, anti-IL-18 mAb and caspase-1 inhibitor partially inhibited the increase in ICAM-1 and CD40 expression induced by doxazosin, prazosin, and terazosin. Doxazosin, prazosin, and terazosin can induce monocyte activation with a specific pattern of expression of adhesion molecules and IL-18 production, and this may lead to T-cell activation through the cell-to-cell interaction. The activation of T cells induced by the increase of the expression of ICAM-1 and CD40 and the production of IL-18 may be involved in the anti-cancer effects of doxazosin, prazosin, and terazosin.
机译：T细胞的激活在抗肿瘤反应中起作用。单核细胞通过诱导细胞间相互作用来激活T细胞，这种相互作用涉及粘附分子与其配体的结合以及IL-18的产生。作者研究了基于喹唑啉的α1-肾上腺素受体拮抗剂布纳唑嗪，多沙唑嗪，吡唑嗪和特拉唑嗪对粘附分子如ICAM-1，B7.1，B7.2，CD40和CD40L在单核细胞上表达的影响来自人外周血单核细胞。多沙唑嗪，哌唑嗪和特拉唑嗪诱导ICAM-1和CD40的表达，但对B7.1，B7.2和CD40L的表达没有影响。此外，在用多沙唑嗪，哌唑嗪和特拉唑嗪处理的温育单核细胞培养基中检测到IL-18。布纳唑嗪不影响粘附分子的表达和IL-18的产生，这表明喹唑啉的化学结构可能与多沙唑嗪，哌唑嗪和特拉唑嗪的作用无关。尽管caspase-1抑制剂完全消除了IL-18的产生，但抗IL-18 mAb和caspase-1抑制剂部分抑制了由多沙唑嗪，哌唑嗪和特拉唑嗪诱导的ICAM-1和CD40表达的增加。多沙唑嗪，哌唑嗪和特拉唑嗪可以诱导单核细胞活化，并具有粘附分子表达和IL-18产生的特定模式，并可能通过细胞间相互作用导致T细胞活化。由ICAM-1和CD40的表达增加引起的T细胞活化以及IL-18的产生可能与多沙唑嗪，哌唑嗪和特拉唑嗪的抗癌作用有关。

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