Ferroptosis in infection, inflammation, and immunity

被引:405
|
作者
Chen, Xin [1 ,2 ]
Kang, Rui [3 ]
Kroemer, Guido [4 ,5 ,6 ,7 ,8 ]
Tang, Daolin [1 ,3 ]
机构
[1] Guangzhou Med Univ, Affiliated Hosp 3, Sch Basic Med Sci, Guangzhou Municipal & Guangdong Prov Key Lab, Guangzhou, Peoples R China
[2] Guangzhou Med Univ, Affiliated Canc Hosp & Inst, Guangzhou, Peoples R China
[3] Univ Texas SouthWestern, Med Ctr, Dept Surg, Dallas, TX USA
[4] Univ Paris, Sorbonne Univ, Inst Natl St & Rech Med, Inst Univ France, Paris, France
[5] Metabol & Cell Biol Platforms, Gustave Roussy Canc Campus, Villejuif, France
[6] Assistance Publ Hosp Paris, Hosp Europeen Georges Pompidou, Ole Biol, Paris, France
[7] Suzhou Inst Syst Biol, Chinese Acad Sci, Suzhou, Peoples R China
[8] Karolinska Univ Hosp, Dept Womens & Childrens Hlth, Stockholm, Sweden
来源
JOURNAL OF EXPERIMENTAL MEDICINE | 2021年 / 218卷 / 06期
基金
欧盟地平线“2020”;
关键词
CELL-DEATH; PROMOTES FERROPTOSIS; LIPID-PEROXIDATION; OXIDATIVE STRESS; B-CELLS; AUTOPHAGY; PATHWAY; MECHANISMS; DAMAGE; IRON;
D O I
10.1084/jem.20210518
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Ferroptosis is a type of regulated necrosis that is triggered by a combination of iron toxicity, lipid peroxidation, and plasma membrane damage. The upstream inducers of ferroptosis can be divided into two categories (biological versus chemical) and activate two major pathways (the extrinsic/transporter versus the intrinsic/enzymatic pathways). Excessive or deficient ferroptotic cell death is implicated in a growing list of physiological and pathophysiological processes, coupled to a dysregulated immune response. This review focuses on new discoveries related to how ferroptotic cells and their spilled contents shape innate and adaptive immunity in health and disease. Understanding the immunological characteristics and activity of ferroptotic death not only illuminates an intersection between cell death and immunity but may also lead to the development of novel treatment approaches for immunopathological diseases.
引用
收藏
页数:15
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