Assessing the Difference Between the Number of CD3+20+ T Cells by Flowcytometry in Idiopathic Nephrotic Syndrome Patients in Relapse and Remission Period: A Pilot Study Assessing the Number of CD3+20+ T Cells in Relapse and Remission Period in INS
Journal of Pediatric Nephrology,
Vol. 11 No. 4 (2023),
5 Bahman 2025
https://doi.org/10.22037/jpn.v11i4.44600
Abstract
Background and Aim: The pathogenesis of idiopathic nephrotic syndrome (INS) remains
unclear. Previously, the INS was assumed a T cell-mediated disease. Cytokines secreted from
T helper 2 cells, reduced T regulatories, which led to activation of T effector cells, resulting
in the increased permeability of glomerulus and nephrotic syndrome. The remedial influence
of B cell depletion by anti-cluster of differentiation marker 20 factors suggests a role of B
cells in the pathogenesis of the disease. However, the exact mechanisms of action of these
medications are unknown. One of these mechanisms is the effect on CD3-20+ T cells.
Methods: A total of 10 patients in relapse of INS and 10 patients in remission were included
in this study. The number of CD3-20+ T cells was calculated by flow cytometry in these two
groups.
Results: In the relapse group, on average, 1.10% of T cells were CD3-20+ cells; in the
remission group, the same data was 0.41%.
Conclusion: The mean number of CD3-20+ T cells in the remission group was lower than
in the relapse group; however, there was no statistical difference between the two groups
- T-lymphocytes
- B-lymphocytes
- Cluster of differentiation markers (CD20 and CD3)
- Flowcytometry
How to Cite
References
Downie ML, Gallibois C, Parekh RS, Noone DG. Nephrotic
syndrome in infants and children: Pathophysiology and management.
Paediatr Int Child Health. 2017; 37(4):248-58. [DOI:1
,1080/20469047.2017.1374003] [PMID]
Kopp JB, Anders HJ, Susztak K, Podestà MA, Remuzzi G,
Hildebrandt F, et al. Podocytopathies. Nat Rev Dis Primers.
; 6(1):68. [DOI:10,1038/s41572-020-0196-7] [PMID]
Hackl A, Zed SEDA, Diefenhardt P, Binz-Lotter J, Ehren
R, Weber LT. The role of the immune system in idiopathic
nephrotic syndrome. Mol Cell Pediatr. 2021; 8(1):18.
[DOI:10,1186/s40348-021-00128-6] [PMID]
Reiser J. Circulating permeability factor suPAR: From concept
to discovery to clinic. Trans Am Clin Climatol Assoc.
; 124:133-8. [PMID]
Königshausen E, Sellin L. Circulating permeability factors
in primary focalsegmental glomerulosclerosis: A review of
proposed candidates. Biomed Res Int. 2016; 2016:3765608.
[DOI:10.1155/2016/3765608] [PMID]
Pukajło-Marczyk A, Zwolińska D. Involvement of hemopexin
in the pathogenesis of proteinuria in children with
idiopathic nephrotic syndrome. J Clin Med. 2021; 10(14):3160.
[DOI:10.3390/jcm10143160] [PMID]
Zhang S, Breidenbach JD, Russell BH, George J, Haller ST.
CD40/CD40L signaling as a promising therapeutic target for
the treatment of renal disease. J Clin Med. 2020; 9(11):3653.
[DOI:10.3390/jcm9113653] [PMID]
Gingele S, Skripuletz T, Jacobs R. Role of CD20+ T cells in
multiple sclerosis: Implications for treatment with ocrelizumab.
Neural Regen Res. 2020; 15(4):663-4. [DOI:10.4103/1673-
266913] [PMID]
Webendörfer M, Reinhard L, Stahl RAK, Wiech T, Mittrücker
HW, Harendza S, et al. Rituximab induces complete remission
of proteinuria in a patient with minimal change disease
and no detectable B Cells. Front Immunol. 2021; 11:586012.
[DOI:10.3389/fimmu.2020.586012] [PMID]
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