Autoimmunity and the Clearance of Dead Cells

被引：707

作者：

Nagata, Shigekazu ^{[1
,2
]}

Hanayama, Rikinari ^{[1
,2
]}

Kawane, Kohki ^{[1
,2
]}

机构：

[1] Kyoto Univ, Grad Sch Med, Dept Med Chem, Sakyo Ku, Kyoto 6068501, Japan

[2] Japan Sci & Technol Corp, Core Res Evolut Sci & Technol, Sakyo Ku, Kyoto 6068501, Japan

来源：

CELL | 2010年 / 140卷 / 05期

关键词：

SYSTEMIC-LUPUS-ERYTHEMATOSUS; CASPASE-ACTIVATED DNASE; TUMOR-NECROSIS-FACTOR; INNATE IMMUNE-RESPONSE; GLOBULE EGF FACTOR-8; RED-BLOOD-CELLS; APOPTOTIC CELLS; PHOSPHATIDYLSERINE RECEPTOR; CAENORHABDITIS-ELEGANS; MACROPHAGE CHEMOTAXIS;

D O I：

10.1016/j.cell.2010.02.014

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

To maintain organismal homeostasis, phagocytes engulf dead cells, which are recognized as dead by virtue of a characteristic "eat me" signal exposed on their surface. The dead cells are then transferred to lysosomes, where their cellular components are degraded for reuse. Inefficient engulfment of dead cells activates the immune system, causing disease such as systemic lupus erythematosus, and if the DNA of the dead cells is not properly degraded, the innate immune response becomes activated, leading to severe anemia and chronic arthritis. Here, we discuss how the endogenous components of dead cells activate the immune system through both extracellular and intracellular pathways. © 2010 Elsevier Inc. All rights reserved.

引用

页码：619 / 630

页数：12

共 125 条

[1] Role of Gas6 receptors in platelet signaling during thrombus stabilization and implications for antithrombotic therapy [J].