Adenosine A3 receptors negatively regulate the engulfment-dependent apoptotic cell suppression of inflammation

来自 NCBI

阅读量:

28

作者:

E DuróA PallaiK K?R?SkényiZ SarangZ Szondy

展开

摘要:

Timed initiation of apoptotic cell death followed by efficient removal mediated by professional macrophages is a key mechanism in maintaining tissue homeostasis. Besides phagocytosis, clearance of apoptotic cells also involves suppression of inflammatory responses by apoptotic cells mediated by both direct inhibition of pro-inflammatory cytokine production and release of soluble anti-inflammatory factors, which act in a paracrine or autocrine fashion to amplify or sustain the anti-inflammatory response. Previous work has demonstrated that during engulfment of apoptotic cells adenosine is produced in sufficient amounts to trigger both adenosine A2A receptors (A2ARs) and A3 receptors (A3Rs). Adenosine bound to A2ARs of macrophages activated the adenylate cyclase pathway to suppress the apoptotic-cell induced, NO-dependent formation of neutrophil migration factors. Here we show by using A3R null engulfing macrophages that the adenosine produced triggers the A3Rs as well, which attenuate the A2AR signaling by inhibiting adenylate cyclase. As a result, the balance in the activation of A2ARs and A3Rs determines the amounts of NO and consequently the levels of neutrophil chemoattractants formed. Since during phagocytosis of apoptotic cells the expression of A2ARs increases, while that of A3Rs decreases, on long term adenosine suppresses the proinflammatory responses in engulfing macrophages.

展开

DOI:

10.1016/j.imlet.2014.06.014

被引量:

30

年份:

2014

通过文献互助平台发起求助,成功后即可免费获取论文全文。

我们已与文献出版商建立了直接购买合作。

你可以通过身份认证进行实名认证,认证成功后本次下载的费用将由您所在的图书馆支付

您可以直接购买此文献,1~5分钟即可下载全文,部分资源由于网络原因可能需要更长时间,请您耐心等待哦~

身份认证 全文购买

相似文献

参考文献

引证文献

来源期刊

研究点推荐

引用走势

2017
被引量:13

站内活动

辅助模式

0

引用

文献可以批量引用啦~
欢迎点我试用!

关于我们

百度学术集成海量学术资源,融合人工智能、深度学习、大数据分析等技术,为科研工作者提供全面快捷的学术服务。在这里我们保持学习的态度,不忘初心,砥砺前行。
了解更多>>

友情链接

百度云百度翻译

联系我们

合作与服务

期刊合作 图书馆合作 下载产品手册

©2025 Baidu 百度学术声明 使用百度前必读

引用