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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
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Related Experiment Video

Updated: May 3, 2026

Isolation and Th17 Differentiation of Na&#239;ve CD4 T Lymphocytes
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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

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Stat3 programs Th17-specific regulatory T cells to control GN.

Malte A Kluger1, Michael Luig1, Claudia Wegscheid2

  • 1III Medizinische Klinik.

Journal of the American Society of Nephrology : JASN
|February 11, 2014
PubMed
Summary
This summary is machine-generated.

Regulatory T cells (Treg17) that suppress Th17 cells are crucial for controlling inflammatory kidney disease. These Treg17 cells require Stat3 for CCR6 expression, enabling their migration to inflamed kidneys.

Keywords:
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Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation
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Area of Science:

  • Immunology
  • Nephrology
  • Cell Biology

Background:

  • Th17 cells are key drivers of inflammatory renal diseases.
  • Mechanisms regulating Th17 cells in kidney inflammation are not fully understood.
  • Th17 lineage-specific regulatory T cells (Treg17) dependent on Stat3 have been identified.

Purpose of the Study:

  • To investigate the function of Treg17 cells in crescentic glomerulonephritis (GN).
  • To elucidate the role of Stat3 and CCR6 in Treg17 cell activity and kidney inflammation.

Main Methods:

  • Utilized the nephrotoxic nephritis (NTN) mouse model.
  • Generated mice with specific Stat3 deficiencies in Treg cells (Foxp3(Cre)×Stat3(fl/fl)).
  • Analyzed Treg cell function, chemokine receptor expression (CCR6), and immune cell trafficking in kidneys.

Main Results:

  • Absence of Treg17 cells exacerbated NTN and promoted Th17 responses.
  • Stat3-deficient Tregs lacked CCR6, impairing their migration to the kidneys.
  • NTN severity was reduced when both Treg17 and Th17 cells were absent.
  • CCR6-expressing Treg17 cells were found in human GN kidney biopsies and STAT3-dependent.

Conclusions:

  • Stat3-dependent Treg17 cells play a critical role in suppressing Th17-mediated crescentic GN.
  • CCR6-mediated migration is essential for Treg17 cell homing to inflamed kidneys.
  • These findings highlight a potential therapeutic target for inflammatory kidney diseases.