New insights into adenosine-receptor-mediated immunosuppression and the role of adenosine in causing the immunodeficiency associated with adenosine deaminase deficiency.

Published

Journal Article (Review)

There is growing interest in manipulating adenosine (Ado) signal transduction to control inflammation and autoimmunity. This concept probably originated with the discovery of severe combined immunodeficiency disease (SCID) in infants with inherited deficiency of adenosine deaminase (ADA). However, the basis for immunosuppression by Ado has not been well defined, and effects of 2'-deoxyadenosine (dAdo), which does not activate Ado receptors, have also been implicated in causing SCID. Here I discuss recent evidence that Ado, acting through its A2A receptor, interferes with NF-kappa B activation in antigen-receptor-stimulated B and T lymphocytes. I also assess the relative contributions of Ado and dAdo to the pathogenesis of ADA-deficient SCID.

Full Text

Duke Authors

Cited Authors

  • Hershfield, MS

Published Date

  • January 2005

Published In

Volume / Issue

  • 35 / 1

Start / End Page

  • 25 - 30

PubMed ID

  • 15580654

Pubmed Central ID

  • 15580654

International Standard Serial Number (ISSN)

  • 0014-2980

Digital Object Identifier (DOI)

  • 10.1002/eji.200425738

Language

  • eng

Conference Location

  • Germany