Regulation of the T Cell Response by CD39

被引:150
|
作者
Takenaka, Maisa C. [1 ]
Robson, Simon [2 ,3 ,4 ]
Quintana, Francisco J. [1 ,5 ]
机构
[1] Harvard Med Sch, Brigham & Womens Hosp, Ann Romney Ctr Neurol Dis, Boston, MA USA
[2] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Med, Div Gastroenterol, Boston, MA USA
[3] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Med, Div Hepatol, Boston, MA USA
[4] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Med, Div Transplantat, Boston, MA USA
[5] Broad Inst MIT & Harva, Cambridge, MA USA
关键词
ARYL-HYDROCARBON RECEPTOR; ATP-DIPHOSPHOHYDROLASE ACTIVITY; HYPOXIA-INDUCIBLE FACTORS; FIND-ME SIGNAL; EXTRACELLULAR ATP; DENDRITIC CELLS; TRANSCRIPTIONAL REGULATION; DIFFERENTIAL EXPRESSION; ADENINE-NUCLEOTIDES; HIGH-SENSITIVITY;
D O I
10.1016/j.it.2016.04.009
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The ectonucleoside triphosphate diphosphohydrolase 1 (ENTPD1, or CD39) catalyzes the phosphohydrolysis of extracellular ATP (eATP) and ADP (eADP) released under conditions of inflammatory stress and cell injury. CD39 generates AMP, which is in turn used by the ecto-5'-nucleotidase CD73 to synthesize adenosine. These ectonucleotidases have a major impact on the dynamic equilibrium of proinflammatory eATP and ADP nucleotides versus immunosuppressive adenosine nucleosides. Indeed, CD39 plays a dominant role in the purinergic regulation of inflammation and the immune response because its expression is influenced by genetic and environmental factors. We review the specific role of CD39 in the kinetic regulation of cellular immune responses in the evolution of disease. We focus on the effects of CD39 on T cells and explore potential clinical applications in autoimmunity, chronic infections, and cancer.
引用
收藏
页码:427 / 439
页数:13
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