CCL28 production in HaCaT cells was mediated by different signal pathways from CCL27
CCL28 production in HaCaT cells was mediated by different signal pathways from CCL27
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DOI：
10.1111/j.1600-0625.2005.00390.x
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发表时间：
2006-02-01
影响因子：
3.6
通讯作者：
Tamaki, K
中科院分区：
文献类型：
--
作者：
Kagami, S;Saeki, H;Tamaki, K
CCL 27和CCL 28都是CCR 10的配体并吸引CCR 10（+）淋巴细胞。我们以前证明，CCL 27和CCL 28强烈表达在血清和皮损角质形成细胞的特应性皮炎和寻常型银屑病患者。然而，角质形成细胞中CCL 27和CCL 28产生的调节尚未得到充分记载。在这项研究中，我们发现，CCL 27和CCL 28的表达和生产的人角质形成细胞系，HaCaT细胞，强烈诱导的炎症细胞因子肿瘤坏死因子-α和白细胞介素-1 β。CCL 27的产生被p38丝裂原活化蛋白激酶和核因子-κ B（NF-κ B）的抑制剂下调。相反，细胞外信号调节激酶和NF-κ B抑制剂下调了CCL 28的产生。我们的研究结果表明，角质形成细胞产生的CCL 28是由不同的信号通路从CCL 27介导的，CCL 27和CCL 28都参与了炎症性皮肤病的发病机制。
Both CCL27 and CCL28 are ligands for CCR10 and attract CCR10(+) lymphocytes. We previously demonstrated that CCL27 and CCL28 were strongly expressed in sera and lesional keratinocytes of patients with atopic dermatitis and psoriasis vulgaris. However, the regulation of CCL27 and CCL28 production in keratinocytes has not been well documented. In this study, we showed that CCL27 and CCL28 expression and production by a human keratinocyte cell line, HaCaT cells, were strongly induced by inflammatory cytokines tumor necrosis factor-alpha and interleukin-1 beta. CCL27 production was downregulated by inhibitors of p38 mitogen-activated protein kinase and nuclear factor-kappa B (NF-kappa B). By contrast, CCL28 production was downregulated by inhibitors of extracellular signal-regulated kinase and NF-kappa B. Our study results suggest that CCL28 produced by keratinocytes is mediated by different signal pathways from CCL27 and that both CCL27 and CCL28 are involved in the pathogenesis of inflammatory skin diseases.