The clearance of dead cells by efferocytosis

被引:555
作者
Boada-Romero, Emilio [1 ]
Martinez, Jennifer [2 ]
Heckmann, Bradlee L. [1 ]
Green, Douglas R. [1 ]
机构
[1] St Jude Childrens Res Hosp, Dept Immunol, 332 N Lauderdale St, Memphis, TN 38105 USA
[2] NIEHS, Inflammat & Autoimmun Grp, Durham, NC USA
基金
美国国家卫生研究院;
关键词
LIVER X RECEPTOR; PATTERN-RECOGNITION RECEPTORS; CHROMATIN PROTEIN HMGB1; CASSETTE TRANSPORTER A1; PANNEXIN; CHANNELS; FIND-ME SIGNALS; APOPTOTIC CELLS; PATHOGEN RECOGNITION; THERAPEUTIC TARGET; LC3-ASSOCIATED PHAGOCYTOSIS;
D O I
10.1038/s41580-020-0232-1
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Multiple modes of cell death have been identified, each with a unique function and each induced in a setting-dependent manner. As billions of cells die during mammalian embryogenesis and daily in adult organisms, clearing dead cells and associated cellular debris is important in physiology. In this Review, we present an overview of the phagocytosis of dead and dying cells, a process known as efferocytosis. Efferocytosis is performed by macrophages and to a lesser extent by other 'professional' phagocytes (such as monocytes and dendritic cells) and 'non-professional' phagocytes, such as epithelial cells. Recent discoveries have shed light on this process and how it functions to maintain tissue homeostasis, tissue repair and organismal health. Here, we outline the mechanisms of efferocytosis, from the recognition of dying cells through to phagocytic engulfment and homeostatic resolution, and highlight the pathophysiological consequences that can arise when this process is abrogated. Development and homeostasis are dependent on rapid cell turnover, achieved by the programmed death and subsequent engulfment and breakdown of cells, a process known as efferocytosis. Defects in efferocytosis have been linked to a wide range of diseases; ongoing research therefore aims to better understand efferocytosis processes so as to uncover new therapeutic targets.
引用
收藏
页码:398 / 414
页数:17
相关论文
共 258 条
[1]   Apoptotic Cells Promote Their Own Clearance and Immune Tolerance through Activation of the Nuclear Receptor LXR [J].
A-Gonzalez, Noelia ;
Bensinger, Steven J. ;
Hong, Cynthia ;
Beceiro, Susana ;
Bradley, Michelle N. ;
Zelcer, Noam ;
Deniz, Jose ;
Ramirez, Cristina ;
Diaz, Mercedes ;
Gallardo, German ;
Ruiz de Galarreta, Carlos ;
Salazar, Jon ;
Lopez, Felix ;
Edwards, Peter ;
Parks, John ;
Andujar, Miguel ;
Tontonoz, Peter ;
Castrillo, Antonio .
IMMUNITY, 2009, 31 (02) :245-258
[2]   Shp1 function in myeloid cells [J].
Abram, Clare L. ;
Lowell, Clifford A. .
JOURNAL OF LEUKOCYTE BIOLOGY, 2017, 102 (03) :657-675
[3]   STING manifests self DNA-dependent inflammatory disease [J].
Ahn, Jeonghyun ;
Gutman, Delia ;
Saijo, Shinobu ;
Barber, Glen N. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2012, 109 (47) :19386-19391
[4]   Pathogen recognition and innate immunity [J].
Akira, S ;
Uematsu, S ;
Takeuchi, O .
CELL, 2006, 124 (04) :783-801
[5]   Phagocytosis of apoptotic cells in homeostasis [J].
Arandjelovic, Sanja ;
Ravichandran, Kodi S. .
NATURE IMMUNOLOGY, 2015, 16 (09) :907-917
[6]   Decreases in CD31 and CD47 Levels on the Cell Surface during Etoposide-Induced Jurkat Cell Apoptosis [J].
Azuma, Yutaro ;
Nakagawa, Hideaki ;
Dote, Kanae ;
Higai, Koji ;
Matsumoto, Kojiro .
BIOLOGICAL & PHARMACEUTICAL BULLETIN, 2011, 34 (12) :1828-1834
[7]   CD24 signalling through macrophage Siglec-10 is a target for cancer immunotherapy [J].
Barkal, Amira A. ;
Brewer, Rachel E. ;
Markovic, Maxim ;
Kowarsky, Mark ;
Barkal, Sammy A. ;
Zaro, Balyn W. ;
Krishnan, Venkatesh ;
Hatakeyama, Jason ;
Dorigo, Oliver ;
Barkal, Layla J. ;
Weissman, Irving L. .
NATURE, 2019, 572 (7769) :392-+
[8]   Engagement of MHC class I by the inhibitory receptor LILRB1 suppresses macrophages and is a target of cancer immunotherapy [J].
Barkal, Amira A. ;
Weiskopf, Kipp ;
Kao, Kevin S. ;
Gordon, Sydney R. ;
Rosental, Benyamin ;
Yiu, Ying Y. ;
George, Benson M. ;
Markovic, Maxim ;
Ring, Nan G. ;
Tsai, Jonathan M. ;
McKenna, Kelly M. ;
Ho, Po Yi ;
Cheng, Robin Z. ;
Chen, James Y. ;
Barkal, Layla J. ;
Ring, Aaron M. ;
Weissman, Irving L. ;
Maute, Roy L. .
NATURE IMMUNOLOGY, 2018, 19 (01) :76-+
[9]   STING Contributes to Abnormal Bone Formation Induced by Deficiency of DNase II in Mice [J].
Baum, Rebecca ;
Sharma, Shruti ;
Organ, Jason M. ;
Jakobs, Christopher ;
Hornung, Veit ;
Burr, David B. ;
Marshak-Rothstein, Ann ;
Fitzgerald, Katherine A. ;
Gravallese, Ellen M. .
ARTHRITIS & RHEUMATOLOGY, 2017, 69 (02) :460-471
[10]  
Baumann I, 2002, ARTHRITIS RHEUM-US, V46, P191, DOI 10.1002/1529-0131(200201)46:1<191::AID-ART10027>3.0.CO