An endogenous caspase-11 ligand elicits interleukin-1 release from living dendritic cells

Author:

Zanoni Ivan123,Tan Yunhao1,Di Gioia Marco1,Broggi Achille1,Ruan Jianbin4,Shi Jianjin5,Donado Carlos A.1,Shao Feng5,Wu Hao46,Springstead James R.7,Kagan Jonathan C.1

Affiliation:

1. Harvard Medical School and Division of Gastroenterology, Boston Children’s Hospital, Boston, MA, USA.

2. Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy.

3. Unit of Cell Signalling and Innate Immunity, Humanitas Clinical and Research Center, Rozzano, Milan, Italy.

4. Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, USA.

5. National Institute of Biological Sciences, Beijing 102206, China.

6. Program in Cellular and Molecular Medicine, Boston Children’s Hospital, Boston, MA, USA.

7. Department of Chemical and Paper Engineering, Western Michigan University, Kalamazoo, MI, USA.

Abstract

Immune activation in context Dendritic cells (DCs) initiate protective immunity upon binding molecules derived from microbes or released from dying cells. Zanoni et al. examined how microbial and endogenous signals interact to shape the course of the ensuing immune response (see the Perspective by Napier and Monack). They found that oxPAPC, an oxidized phospholipid released from dying cells, binds to a protein called caspase-11 in DCs, activating an inflammatory program in these cells. Whereas caspase-11 binding to oxPAPC and bacterial lipopolysaccharide causes DCs to produce the cytokine interleukin-1 (IL-1) and undergo cell death, binding to oxPAPC alone triggers DCs to secrete IL-1 and induce strong adaptive immunity. Thus, context-dependent signals can shape the ensuing immune response. Science , this issue p. 1232 ; see also p. 1173

Funder

Mead Johnson & Company

Burroughs Wellcome Fund

Harvard Digestive Diseases Center

Cariplo Foundation

Jane Coffin Childs Fund

NIH

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3