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Related Concept Videos

T Cell Types and Functions01:24

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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.
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Updated: Oct 25, 2025

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
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STAT5 Represses a STAT3-Independent Th17-like Program during Th9 Cell Differentiation.

D Alejandro Canaria1, Bingyu Yan2, Maia G Clare1

  • 1Department of Biological Sciences, Purdue University, West Lafayette, IN.

Journal of Immunology (Baltimore, Md. : 1950)
|August 5, 2021
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Interleukin-2 (IL-2) signaling via STAT5 is crucial for controlling T helper 9 (Th9) cell differentiation and preventing a Th17-like signature. This balance is key in allergic diseases.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • T helper 9 (Th9) cells are involved in immunity and allergic diseases.
  • Th9 differentiation requires IL-4, TGF-β, and IL-2, with IL-2/STAT5 signaling playing a key role.
  • The precise roles of STAT5 in Th9 cell development, including gene repression, are not fully understood.

Purpose of the Study:

  • To investigate the role of IL-2/STAT5 signaling in regulating Th9 cell differentiation and its balance with Th17-like cell programs.
  • To elucidate the mechanisms by which STAT5 influences gene expression during Th9 cell development.

Main Methods:

  • Analysis of human allergy-associated Th9 cells for STAT5-mediated gene repression signatures.
  • Murine Th9 cell differentiation experiments with IL-2/STAT5 signaling blockade.
  • Assessment of IL-17 and Rorγt expression under varying IL-2 conditions.
  • Investigating the roles of STAT3, Rorγt, and BATF in IL-17 production and cell survival.

Main Results:

  • Human Th9 cells show STAT5-mediated gene repression, silencing a Th17-like signature.
  • Blocking IL-2/STAT5 signaling in murine Th9 cells induces IL-17 and Rorγt expression.
  • IL-17 production in IL-2-deprived Th9 cells is STAT3-independent but requires Rorγt and BATF.
  • STAT3 is essential for the prolonged survival of IL-17-producing cells, even when differentiation is STAT3-independent.

Conclusions:

  • IL-2/STAT5 signaling is critical for maintaining the balance between Th9 and Th17-like cell differentiation.
  • STAT5-mediated repression by IL-2 signaling helps prevent Th17-like cell development in Th9 cells.
  • These findings have implications for understanding and potentially treating allergic diseases.