Regulation of the T Cell Response by CD39
Trends in Immunology, ISSN: 1471-4906, Vol: 37, Issue: 7, Page: 427-439
2016
- 153Citations
- 252Captures
- 1Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations153
- Citation Indexes153
- 153
- CrossRef104
- Captures252
- Readers252
- 252
- Mentions1
- References1
- 1
Review Description
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.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S147149061630031X; http://dx.doi.org/10.1016/j.it.2016.04.009; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84969641306&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/27236363; https://linkinghub.elsevier.com/retrieve/pii/S147149061630031X; http://linkinghub.elsevier.com/retrieve/pii/S147149061630031X
Elsevier BV
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