Regulatory T cells and oxidative stress in minimal change nephropathy

Research output: Chapter in Book/Report/Conference proceedingChapter


Minimal change nephropathy (MCN) in children has been historically considered a T-cell disorder; however, evolution in basic immunology contributed to suggest a more articulated cell interaction. There is a general consensus that CD4+ cells decrease and CD8+ and NK cells increase during relapse of proteinuria. Combined modification of the B-cell compartment is now emerging as an unexpected finding from studies utilizing anti-CD20 monoclonal antibodies as therapeutic approach. Modification of the balance between T-helper 17 cell (Th17) and regulatory T cell (Treg) is also considered as a peculiar characteristic of MCN and highlights a potential key role of regulatory T and B cells. The direct trigger is still unknown: the general idea is that a single factor or a cytokine per se cannot be considered pathogenic of MCN and that a complex array of molecules and cells may better explain the pathology. Innate immunity by means of soluble factor (LPS) or oxidants may be the first event. Tregs could be involved in MCN as a second step in a cascade where the first hit remains unidentified. The evidence of a Treg involvement in MCN is entirely based on results coming from experimental nephrosis (i.e., in Buffalo/Mna rats, Adriamycin nephrosis, and LPS). Regulatory molecules such as ATP/adenosine play a switch-off effect on Treg, and co-stimulatory CD80 expressed by both B cells and activated/regulatory T cells could explain the complex interplay.

Original languageEnglish
Title of host publicationMolecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome
PublisherSpringer Japan
Number of pages38
ISBN (Print)9784431552703, 9784431552697
Publication statusPublished - Jan 1 2016


  • B cells
  • Minimal change nephropathy
  • Nephrotic syndrome
  • Regulatory T cells
  • Rituximab

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)


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