Regulation of innate immunity by the nucleotide pathway in children with idiopathic nephrotic syndrome

R. Bertelli, M. Bodria, M. Nobile, S. Alloisio, R. Barbieri, G. Montobbio, P. Patrone, G. M. Ghiggeri

Research output: Contribution to journalArticlepeer-review


Activation of the oxidative burst and failure of CD4 +CD25 + cell regulation have been implicated in idiopathic nephrotic syndrome (iNS). The intimate mechanism is, however, unknown and requires specifically focused studies. We investigated reactive oxygen species (ROS) generation [di-chlorofluorescein-diacetate (DCFDA)] fluorescence assay and the regulatory adenosine 5′-triphosphate (ATP) pathways in the blood of 41 children with iNS, utilizing several agonists and antagonists of nucleotide/nucleoside receptors, including the addition of soluble apyrase. The CD4 +CD25 +CD39 +/CD73 + expression was determined in vivo in parallel during disease activity. Overall, we found that the percentage of CD39 +CD4 +CD25 + was reduced markedly in iNS by 80% (3·43±0·04% versus 13·14±0·07% of total lymphocytes, P+CD25 +, with higher rates in patients with very low CD39 +CD4 +CD25 + levels (+CD4 +CD25 + expression in iNS highlights an impairment of ATP degradation in this pathology. However, high ROS surviving ATP consumption implies a major role of other regulatory pathways.

Original languageEnglish
Pages (from-to)55-63
Number of pages9
JournalClinical and Experimental Immunology
Issue number1
Publication statusPublished - Oct 2011


  • Adenosine
  • ATP regulatory pathway
  • Free radicals
  • Innate immunity
  • Nephrotic syndrome
  • Oxidation burst
  • Proteinuria

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy


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