In vivo expression of interleukin-8, and regulated on activation, normal, T-cell expressed, and secreted, by human germinal centre B lymphocytes.
In vivo expression of interleukin-8, and regulated on activation, normal, T-cell expressed, and secreted, by human germinal centre B lymphocytes.
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IL-8 的体内表达，并调节人生发中心 B 淋巴细胞的激活、正常 T 细胞表达和分泌。
DOI：
10.1046/j.1365-2567.2003.01745.x
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发表时间：
2003
期刊：
影响因子：
6.4
通讯作者：
Martinez-Valdez,Hector
中科院分区：
文献类型：
--
作者：
Sims-Mourtada,JenniferC;Guzman-Rojas,Liliana;Rangel,Roberto;Nghiem,DatX;Ullrich,StephenE;Guret,Christiane;Cain,Kelly;Martinez-Valdez,Hector
生发中心（GCs）内的T细胞归巢是体液B细胞应答所必需的。然而，涉及T细胞募集到GC的机制尚不完全清楚。通过免疫组织学、Northern和Western blot，我们发现人GC B淋巴细胞可以表达CxC和CC趋化因子。此外，B细胞亚群特异性实验显示，白细胞介素(IL) - 8和受激活、正常、T细胞表达和分泌（RANTES）调控的白细胞介素(IL) - 8主要由GC中心母细胞和中心细胞表达，这表明趋化因子的表达在B淋巴细胞与T淋巴细胞进行抗原依赖性活性相互作用的阶段是必不可少的。根据这一假设，我们发现招募到GC中的T细胞相关表达IL - 8和RANTES受体。我们认为趋化因子表达是促进T淋巴细胞募集到GCs并支持同源B细胞：T细胞相遇的关键B细胞功能。此外，我们的数据与缺乏CC和CxC趋化因子或其受体的小鼠的T细胞向次级淋巴器官的归巢受损是一致的。
T‐cell homing within germinal centres (GCs) is required for humoral B‐cell responses. However, the mechanisms implicated in the recruitment of T cells into the GC are not completely understood. Here we show, by immunohistology, and Northern and Western blots, thatin vivohuman GC B lymphocytes can express CxC and CC chemokines. Moreover, B‐cell subset‐specific experiments reveal that interleukin (IL)‐8 and regulated on activation, normal, T‐cell expressed, and secreted (RANTES) are predominantly expressed by GC centroblast and centrocytes, suggesting that chemokine expression is essential at stages in which B‐lymphocytes engage in active antigen‐dependent interactions with T lymphocytes. In keeping with this hypothesis, we show that the T cells recruited into the GC correlatively express the receptors for IL‐8 and RANTES. We propose that chemokine expression is a key B‐cell function that facilitates T‐lymphocyte recruitment into the GCs and supports cognate B‐cell : T‐cell encounters. Moreover, our data are consistent with the impaired homing of T cells to secondary lymphoid organs in mice that are either deficient in CC and CxC chemokines or their receptors.