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Published on: September 26, 2013
Th1/Th2 balance in childhood idiopathic nephrotic syndrome
K Kaneko1, K Tuchiya, S Fujinaga
1Department of Pediatrics, Juntendo University School of Medicine, Tokyo, Japan. kkaneko@med.juntendo.ac.jp
Insights
This study found no significant imbalance in helper T cell type 1 (Th1) or type 2 (Th2) cytokines in children with idiopathic nephrotic syndrome (INS). The immunological abnormality in INS likely involves other immune cells, not helper T cells.
Area of Science:
- Immunology
- Pediatrics
- Nephrology
Background:
- Childhood idiopathic nephrotic syndrome (INS) has conflicting evidence regarding T helper cell type 1 (Th1) and type 2 (Th2) cytokine profiles.
- Understanding the Th1/Th2 balance is crucial for elucidating the immunological pathogenesis of INS.
Purpose of the Study:
- To investigate the balance of Th1 and Th2 helper T cells in children with INS.
- To compare intracellular cytokine production of interferon-gamma (IFNγ) and interleukin-4 (IL-4) in CD4+ cells between INS patients and healthy controls.
Main Methods:
- A cohort of 16 children with steroid-sensitive INS and 15 healthy children were studied.
- Three-color flow cytometry was employed to measure intracellular IFNγ and IL-4 production in CD4+ T cells.
Main Results:
- No significant differences were observed in the percentages of Th0, Th1, or Th2 cells within CD4+ cells in children with INS compared to controls.
- The Th1/Th2 ratio in INS patients did not differ between nephrotic relapse and remission phases, nor compared to healthy children.
Conclusions:
- The findings suggest that the Th1/Th2 balance is not significantly skewed in childhood INS.
- The primary immunological abnormality in INS may reside in other immune cells, such as suppressor/cytotoxic T cells, NK cells, or monocytes/macrophages.
- Further research on these alternative cell types is warranted to clarify the pathogenesis of INS.
Aims:
In view of the conflicting evidence of helper T cell type 1 (Th1) or type 2 (Th2) pattern of cytokine synthesis in childhood idiopathic nephrotic syndrome (INS) this study examined the balance of Th1 and Th2 which are characterized by intracellular cytokine production of interferon-gamma (IFNgamma) and interleukin-4 (IL-4), respectively.
Subjects And Methods:
Sixteen children with steroid-sensitive INS (mean age 9.0 years) were included in this study, together with 15 healthy normal children (mean age 7.9 years) for the control group. Intracellular production of both IFNgamma and IL-4 in helper T cell (CD4+ cell) was investigated by a 3-color flow cytometry.
Results:
The cross-sectional data showed no significant differences of percentages of Th0 (IFNgamma+ IL-4+ CD4+ cell), Th1 (IFNgamma+ lL-4- CD4+ cell) and Th2 (IFNgamma- IL-4+ CD4+ cell) in CD4+ cells (p > 0.05). The Th1/Th2 ratio during nephrotic relapse did not differ from those during nephrotic remission and in normal healthy children (p > 0.05).
Conclusion:
We conclude that there is no significant skew of Th1/Th2 balance in childhood INS and that the cardinal immunological abnormality does not lie in helper T cells but in other cells, such as suppressor/cytotoxic T cells, natural killer cells or monocytes/macrophage. To clarify the pathogenesis of INS, comprehensive studies for these cells would be worthwhile.
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