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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >IL-8 secreted in a macrophage migration-inhibitory factor- and CD74-dependent manner regulates B cell chronic lymphocytic leukemia survival
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IL-8 secreted in a macrophage migration-inhibitory factor- and CD74-dependent manner regulates B cell chronic lymphocytic leukemia survival

机译：以巨噬细胞迁移抑制因子和CD74依赖性方式分泌的IL-8调节B细胞慢性淋巴细胞性白血病的存活

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摘要

Chronic lymphocytic leukemia (CLL) is a malignant disease of small mature lymphocytes. Previous studies have shown that CLL B lymphocytes express relatively large amounts of CD74 mRNA relative to normal B cells. In the present study, we analyzed the molecular mechanism regulated by CD74 in B-CLL cells. The results presented here show that activation of cell-surface CD74, expressed at high levels from an early stage of the disease by its natural ligand, macrophage migration-inhibition factor (MIF), initiates a signaling cascade that contributes to tumor progression. This pathway induces NF-κB activation, resulting in the secretion of IL-8 which, in turn, promotes cell survival. Inhibition of this pathway leads to decreased cell survival. These findings could form the basis of unique therapeutic strategies aimed at blocking the CD74-induced, IL-8- dependent survival pathway.
机译：慢性淋巴细胞性白血病（CLL）是小型成熟淋巴细胞的恶性疾病。先前的研究表明，相对于正常B细胞​​，CLL B淋巴细胞表达相对大量的CD74 mRNA。在本研究中，我们分析了CD74调控B-CLL细胞的分子机制。此处显示的结果表明，从疾病的早期开始就通过其天然配体巨噬细胞迁移抑制因子（MIF）高水平表达的细胞表面CD74被激活，从而启动了一个信号级联，有助于肿瘤的进展。该途径诱导NF-κB活化，导致IL-8分泌，进而促进细胞存活。该途径的抑制导致细胞存活降低。这些发现可能构成旨在阻断CD74诱导的IL-8依赖性生存途径的独特治疗策略的基础。

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