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首页> 外文期刊>Nature immunology >Fever-range thermal stress promotes lymphocyte trafficking across high endothelial venules via an interieukin 6 trans-signaling mechanism
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Fever-range thermal stress promotes lymphocyte trafficking across high endothelial venules via an interieukin 6 trans-signaling mechanism

机译：发烧范围的热应激通过白细胞介素6的信号转导机制促进淋巴细胞跨高内皮微血管的运输

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摘要

Fever is an evolutionarily conserved response during acute inflammation, although its physiological benefit is poorly understood. Here we show thermal stress in the range of fever temperatures increased the intravascular display of two 'gatekeeper' homing molecules, intercellular adhesion molecule 1 (ICAM-1) and CCL21 chemokine, exclusively in high endothelial venules (HEVs) that are chief portals for the entry of blood-borne lymphocytes into lymphoid organs. Enhanced endothelial expression of ICAM-1 and CCL21 was linked to increased lymphocyte trafficking across HEVs. A bifurcation in the mechanisms controlling HEV adhesion was demonstrated by evidence that the thermal induction of ICAM-1 but not of CCL21 involved an interleukin 6 trans. signaling pathway. Our findings identify the 'HEV axis' as a thermally sensitive alert system that heightens immune surveillance during inflammation by amplifying lymphocyte trafficking to lymphoid organs.
机译：发烧是急性炎症过程中进化上保守的反应，尽管对其生理益处知之甚少。在这里，我们显示出在发烧温度范围内的热应力增加了两个“关守”归巢分子，细胞间粘附分子1（ICAM-1）和CCL21趋化因子的血管内显示，这些分子专门存在于高内皮小静脉（HEV）中，而高内皮小静脉是它们的主要门户血源性淋巴细胞进入淋巴器官。 ICAM-1和CCL21的内皮表达增强与跨HEV的淋巴细胞运输增加有关。通过证据表明ICAM-1的热诱导而不涉及CCL21的热诱导涉及白介素6反式，证明了控制HEV粘附的机制分叉。信号通路。我们的发现将“ HEV轴”识别为热敏警报系统，可通过放大淋巴细胞向淋巴器官的运输来增强炎症过程中的免疫监测。

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