CD39 and CD73 in immunity and inflammation

被引：928

作者：

Antonioli, Luca ^{[1
,2
,3
]}

Pacher, Pal ^{[4
]}

Vizi, E. Sylvester ^{[5
,6
]}

Hasko, Gyoergy ^{[2
,3
]}

机构：

[1] Univ Pisa, Dept Clin & Expt Med, I-56126 Pisa, Italy

[2] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Surg, Newark, NJ 07103 USA

[3] Univ Med & Dent New Jersey, New Jersey Med Sch, Ctr Immun & Inflammat, Newark, NJ 07103 USA

[4] NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA

[5] Hungarian Acad Sci, Inst Expt Med, H-1450 Budapest, Hungary

[6] Semmelweis Univ, Dept Pharmacol & Pharmacotherapy, H-1445 Budapest, Hungary

来源：

TRENDS IN MOLECULAR MEDICINE | 2013年 / 19卷 / 06期

基金：

美国国家卫生研究院;

关键词：

cytokine; Treg; macrophage; neutrophil; sepsis; CD39; CD73; ectonucleotidase; REGULATORY T-CELLS; ECTO-5'-NUCLEOTIDASE CD73; EXTRACELLULAR ADENOSINE; ISCHEMIA-REPERFUSION; TUMOR-GROWTH; NUCLEOTIDE PHOSPHOHYDROLYSIS; ECTONUCLEOTIDASE CD39; NEUTROPHIL CHEMOTAXIS; PROGNOSTIC BIOMARKER; CATALYTIC-PROPERTIES;

D O I：

10.1016/j.molmed.2013.03.005

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：

The enzymatic activities of CD39 and CD73 play strategic roles in calibrating the duration, magnitude, and chemical nature of purinergic signals delivered to immune cells through the conversion of ADP/ATP to AMP and AMP to adenosine, respectively. This drives a shift from an ATP-driven proinflammatory environment to an anti-inflammatory milieu induced by adenosine. The CD39/CD73 pathway changes dynamically with the pathophysiological context in which it is embedded. It is becoming increasingly appreciated that altering this catabolic machinery can change the course or dictate the outcome of several pathophysiological events, such as AIDS, autoimmune diseases, infections, atherosclerosis, ischemia-reperfusion injury, and cancer, suggesting these ectoenzymes are novel therapeutic targets for managing a variety of disorders.

引用

页码：355 / 367

页数：13

共 173 条

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