impact factor
logo
 

Reviews

 

The adenosinergic system: a potential player in the pathogenesis of ANCA-associated vasculitis?


1, 2, 3, 4

 

  1. Vth Department of Medicine (Nephrology/Endocrinology/Rheumatology), University Medical Centre Mannheim, University of Heidelberg, Mannheim, Germany.
  2. Vth Department of Medicine (Nephrology/Endocrinology/Rheumatology), University Medical Centre Mannheim, University of Heidelberg, Mannheim, Germany.
  3. Vth Department of Medicine (Nephrology/Endocrinology/Rheumatology), University Medical Centre Mannheim, University of Heidelberg, Mannheim, Germany.
  4. Vth Department of Medicine (Nephrology/Endocrinology/Rheumatology), University Medical Centre Mannheim, University of Heidelberg, Mannheim, Germany. anna-isabelle.kaelsch@umm.de

CER10921
2018 Vol.36, N°2 ,Suppl.111
PI 0143, PF 0151
Reviews

Free to view
(click on article PDF icon to read the article)

PMID: 29745882 [PubMed]

Received: 26/10/2017
Accepted : 01/02/2018
In Press: 03/05/2018
Published: 18/05/2018

Abstract

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a potentially lethal autoimmune disease whose pathology comprises disturbed T cell differentiation and functionality accompanied by dysfunctional autoreactive immunoglobulin development, culminating in destructive innate immune response as well. Purines, adenine nucleotides and adenosine in particular, have been elucidated as potent extracellular mediators for fine adjustment of these pivotal processes establishing human immunity. Therefore, the extracellular purinergic microenvironment is under control of ectonucleotidases CD39 and CD73 degrading pro-inflammatory adenosine triphosphate (ATP) to anti-inflammatory adenosine as well as adenosine deaminase bound to CD26 deactivating adenosine. Accordingly, the ATP P2X7 receptor was elicited to be responsible for promotion of inflammation, while predominantly the adenosine A2A receptor demonstrated the opposite. Recent reports pointed at the adenosinergic system to be crucially involved in AAV pathogenesis. Here, experimental evidence on ecto-enzymes controlling extracellular adenine nucleotide concentrations and purinergic signaling in the immune system with respect to its contribution to the AAV pathomechanism is reviewed besides unsolved problems being identified that require further investigation in order to develop new treatment strategies for AAV.

Rheumatology Article