Human adenosine deaminases ADA1 and ADA2 bind to different subsets of immune cells View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2016-09-23

AUTHORS

Yuliia Kaljas, Chengqian Liu, Maksym Skaldin, Chengxiang Wu, Qing Zhou, Yuanan Lu, Ivona Aksentijevich, Andrey V. Zavialov

ABSTRACT

At sites of inflammation and tumor growth, the local concentration of extracellular adenosine rapidly increases and plays a role in controlling the immune responses of nearby cells. Adenosine deaminases ADA1 and ADA2 (ADAs) decrease the level of adenosine by converting it to inosine, which serves as a negative feedback mechanism. Mutations in the genes encoding ADAs lead to impaired immune function, which suggests a crucial role for ADAs in immune system regulation. It is not clear why humans and other mammals possess two enzymes with adenosine deaminase activity. Here, we found that ADA2 binds to neutrophils, monocytes, NK cells and B cells that do not express CD26, a receptor for ADA1. Moreover, the analysis of CD4+ T-cell subset revealed that ADA2 specifically binds to regulatory T cells expressing CD39 and lacking the receptor for ADA1. Also, it was found that ADA1 binds to CD16− monocytes, while CD16+ monocytes preferably bind ADA2. A study of the blood samples from ADA2-deficient patients showed a dramatic reduction in the number of lymphocyte subsets and an increased concentration of TNF-α in plasma. Our results suggest the existence of a new mechanism, where the activation and survival of immune cells is regulated through the activities of ADA2 or ADA1 anchored to the cell surface. More... »

PAGES

555-570

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00018-016-2357-0

DOI

http://dx.doi.org/10.1007/s00018-016-2357-0

DIMENSIONS

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PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27663683


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82 inflammation
83 lead
84 levels
85 levels of adenosine
86 local concentration
87 lymphocyte subsets
88 mammals
89 mechanism
90 monocytes
91 mutations
92 nearby cells
93 negative feedback mechanism
94 neutrophils
95 new mechanism
96 number
97 patients
98 plasma
99 receptors
100 reduction
101 regulation
102 response
103 results
104 role
105 samples
106 sites
107 sites of inflammation
108 study
109 subset
110 surface
111 survival
112 system regulation
113 tumor growth
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