巨噬细胞中IL-10信号的丢失限制了前列腺素E2驱动的细菌杀伤

The Tokushima journal of experimental medicine Pub Date : 2019-12-05 DOI:10.1084/jem.20180649

S. Mukhopadhyay, E. Heinz, I. Porreca, K. Alasoo, Amy T. Y. Yeung, Huei-Ting Yang, T. Schwerd, J. Forbester, C. Hale, Chukwuma A. Agu, Yoon Ha Choi, Julia Rodrigues, M. Capitani, L. Jostins-Dean, D. Thomas, S. Travis, Daniel J. Gaffney, W. Skarnes, N. Thomson, H. Uhlig, G. Dougan, F. Powrie

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引用次数: 41

摘要

细胞因子和脂质介质是炎症的关键调节因子;但人们对它们之间的机械联系知之甚少。在这里，Mukhopadhyay等人展示了细胞因子IL-10和脂质介质PGE2之间的一种新的调节，在功能上将它们与肠道炎症联系起来。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Loss of IL-10 signaling in macrophages limits bacterial killing driven by prostaglandin E2

Cytokines and lipid mediators are key regulators of inflammation; but how they are mechanistically linked is poorly understood. Here, Mukhopadhyay et al. show a novel regulation between cytokine IL-10 and lipid mediator PGE2 that functionally connects them to intestinal inflammation.

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The Tokushima journal of experimental medicine

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