Murine mammary carcinoma cells and CD11c+ dendritic cells elicit distinct responses to lipopolysaccharide and exhibit differential expression of genes required for TLR4 signaling
Murine mammary carcinoma cells and CD11c+ dendritic cells elicit distinct responses to lipopolysaccharide and exhibit differential expression of genes required for TLR4 signaling
复制标题
DOI：
10.1016/j.cellimm.2010.08.015
复制
发表时间：
2010-01-01
影响因子：
4.3
通讯作者：
Kurt, Robert A.
中科院分区：
文献类型：
--
作者：
De Sousa, Chiquita Palha;Blum, Christopher M.;Kurt, Robert A.
虽然TLR经常在DC上进行研究，因为它们能够桥接先天性和适应性防御，但TLR也由上皮细胞表达。由于大多数癌症是癌，因此是上皮起源的，我们想知道癌和DC是否对TLR激动剂有相似的反应。我们发现乳腺癌4 T1和CD 11 c（+）DC都能在TLR 4激动剂脂多糖（LPS）作用下分泌促炎趋化因子。然而，存在着明显的二分法。DC分泌IL-1 β，而4 T1不分泌IL-1 β。INF-α，并上调LPS处理后的CD 80和CD 86表达。差异反应性的一个潜在原因是DC表达更高水平的TLR 4、CD 14、Myd 88和TRAM。尽管TLR信号传导蛋白水平低，但癌能够引起一系列反应，这取决于TLR激动剂治疗的来源、剂量、长度和频率。因此，癌和DC对LPS有明显的反应。(C)2010年爱思唯尔公司All rights reserved.
Although TLR are often studied on DC because of their ability to bridge innate and adaptive defenses, TLR are also expressed by epithelial cells. Because the majority of cancers are carcinomas, and thus of epithelial origin, we wanted to know whether a carcinoma and DC responded similarly to a TLR agonist. We found the mammary carcinoma 4T1 and CD11c(+) DC both secreted proinflammatory chemokines in response to the TLR4 agonist lipopolysaccharide (LPS). However a clear dichotomy existed. DC, but not 4T1 secreted IL-1 beta. INF-alpha, and upregulated CD80 and CD86 expression following LPS treatment. A potential reason for differential responsiveness was that DC expressed greater levels of TLR4, CD14, Myd88, and TRAM. Despite the low level of TLR signaling proteins, the carcinoma were able to elicit a range of responses contingent upon the source, dose, length, and frequency of TLR agonist treatment. Thus, carcinoma and DC are distinctly responsive to LPS. (C) 2010 Elsevier Inc. All rights reserved.