The role of adenosinergic pathway in human autoimmune diseases

Autoimmune diseases are characterized by the abnormal immune response against self-tissue, which are caused by the failure of nature immune homeostasis. Nature immune homeostasis represents the normal state of appropriate immune response to nonself-antigen and unresponsiveness to self-antigens. In n...

Full description

Saved in:
Bibliographic Details
Published inImmunologic Research Vol. 64; no. 5-6; pp. 1133 - 1141
Main Authors Dong, Ke, Gao, Zhao-wei, Zhang, Hui-zhong
Format Journal Article Book Review
LanguageEnglish
Published New York Springer US 01.12.2016
Springer Nature B.V
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Autoimmune diseases are characterized by the abnormal immune response against self-tissue, which are caused by the failure of nature immune homeostasis. Nature immune homeostasis represents the normal state of appropriate immune response to nonself-antigen and unresponsiveness to self-antigens. In normal situation, immune homeostasis is regulated by immunosuppressive signal and immunostimulating signal together. Accumulating data have demonstrated that the adenosinergic pathway played key roles in immune suppression and shield body from an excessive inflammatory response. The deficiency of adenosinergic pathway results in the imbalance between the pro- and anti-inflammatory activities. Thus, researchers pay much attention to the role of adenosinergic pathway in autoimmune diseases development. To date, accumulating data have suggested an important role of adenosinergic pathway-related molecules (i.e., CD39, CD73, ADA, adenosine receptors, etc.) in many types of human autoimmune diseases. More importantly, these findings have presented potential value of adenosinergic pathway analysis to be used for autoimmune diseases diagnosis, monitoring and treatment. In this review, we will provide a comprehensive description of the role of adenosinergic pathway in human autoimmune diseases.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ObjectType-Article-1
ObjectType-Feature-2
ISSN:0257-277X
1559-0755
DOI:10.1007/s12026-016-8870-2