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首页> 外文期刊>Cytokine >Regulation of a lymphocyte-endothelial-IL-6 trans-signaling axis by fever-range thermal stress: hot spot of immune surveillance.
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Regulation of a lymphocyte-endothelial-IL-6 trans-signaling axis by fever-range thermal stress: hot spot of immune surveillance.

机译：发热范围的热应激对淋巴细胞-内皮-IL-6反信号轴的调节：免疫监视的热点。

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摘要

The pleiotropic cytokine, interleukin-6 (IL-6), has emerged in recent years as a key regulator of the transition from innate to adaptive immunity through its ability to modulate leukocyte recruitment at inflammatory sites. This review highlights a newly identified role for IL-6 trans-signaling, initiated by an agonistic complex of IL-6 and a soluble form of IL-6 receptor alpha, in heightening immune surveillance of peripheral lymphoid organs during febrile inflammatory responses. Inflammatory cues provided by the thermal component of fever trigger IL-6 trans-signaling to act at discrete levels in the multistep adhesion cascade that governs the entry of blood-borne lymphocytes across 'gatekeeper' high endothelial venules (HEVs) in lymph nodes and Peyer patches. IL-6 trans-signaling-dependent mechanisms have been elucidated during thermal stimulation of primary tethering and rolling of lymphocytes along the lumenal surface of HEVs as well as during secondary firm arrest of lymphocytes in HEVs prior to their migration into the underlying parenchyma. These mechanisms profoundly increase the probability that lymphocytes that continuously patrol the body will engage in productive encounters with target antigens sequestered within lymphoid organs. Findings that the lymphocyte-HEV-IL-6 trans-signaling biological axis functions as a thermally-sensitive alert system that promotes immune surveillance provide insight into one of the unresolved mysteries in immunology regarding the benefits of mounting a febrile reaction during inflammation.
机译：近年来，多效性细胞因子白介素6（IL-6）作为其从先天免疫向适应性免疫过渡的关键调节剂，通过其调节炎症部位白细胞募集的能力而出现。这篇综述着重指出了由IL-6的激动性复合物和IL-6受体α的可溶性形式引发的IL-6反信号的新发现的作用，它在发热性炎症反应期间增强了外周淋巴器官的免疫监视。发烧热成分提供的炎症线索触发IL-6反信号转导，作用于多步粘附级联反应中的离散水平，从而控制血源性淋巴细胞穿过淋巴结和淋巴结中的“关守”高内皮小静脉（HEV）进入补丁。已经阐明了在热刺激初次束缚和沿HEV腔表面滚动淋巴细胞的过程中，以及在HEV迁移至下面的实质之前，淋巴细胞继发牢固停滞的过程中，IL-6反信号依赖性机制。这些机制极大地增加了连续巡逻身体的淋巴细胞与螯合在淋巴器官内的靶抗原进行有效接触的可能性。淋巴细胞-HEV-IL-6信号转导生物轴起促进免疫监视的热敏警报系统的作用，发现了关于免疫学中尚未解决的谜团之一的知识，该谜团涉及在炎症过程中进行高热反应的益处。

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