Abstract
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 language | English |
|---|---|
| Title of host publication | Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome |
| Publisher | Springer Japan |
| Pages | 105-142 |
| Number of pages | 38 |
| ISBN (Print) | 9784431552703, 9784431552697 |
| DOIs | |
| Publication status | Published - Jan 1 2016 |
Fingerprint
Keywords
- B cells
- Minimal change nephropathy
- Nephrotic syndrome
- Regulatory T cells
- Rituximab
ASJC Scopus subject areas
- Medicine(all)
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
Regulatory T cells and oxidative stress in minimal change nephropathy. / Bertelli, Roberta; Di Donato, Armando; Bonanni, Alice; Rossi, Roberta; Ghiggeri, Gian Marco.
Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome. Springer Japan, 2016. p. 105-142.Research output: Chapter in Book/Report/Conference proceeding › Chapter
}
TY - CHAP
T1 - Regulatory T cells and oxidative stress in minimal change nephropathy
AU - Bertelli, Roberta
AU - Di Donato, Armando
AU - Bonanni, Alice
AU - Rossi, Roberta
AU - Ghiggeri, Gian Marco
PY - 2016/1/1
Y1 - 2016/1/1
N2 - 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.
AB - 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.
KW - B cells
KW - Minimal change nephropathy
KW - Nephrotic syndrome
KW - Regulatory T cells
KW - Rituximab
UR - http://www.scopus.com/inward/record.url?scp=84956553370&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84956553370&partnerID=8YFLogxK
U2 - 10.1007/978-4-431-55270-3_7
DO - 10.1007/978-4-431-55270-3_7
M3 - Chapter
AN - SCOPUS:84956553370
SN - 9784431552703
SN - 9784431552697
SP - 105
EP - 142
BT - Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome
PB - Springer Japan
ER -