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Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
Published on: April 16, 2015
Late developmental plasticity in the T helper 17 lineage
Yun Kyung Lee1, Henrietta Turner, Craig L Maynard
1Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Immunity
|January 3, 2009
Summary
Transforming growth factor-beta (TGF-β) is crucial for T helper 17 (Th17) cell development and sustained IL-17 production. In its absence, Th17 cells can shift to produce IFN-gamma, impacting autoimmunity and host defense.
Area of Science:
- Immunology
- Cellular and Molecular Immunology
- T cell differentiation
Background:
- T helper 17 (Th17) cells are critical immune cells involved in host defense and autoimmunity.
- Th17 cell development requires transforming growth factor-beta (TGF-β) and interleukin-6 (IL-6).
- While Th17 cells produce IL-17, interferon-gamma (IFN-γ)-producing T cells are also observed, and STAT4/T-bet deficient mice are protected from Th17-associated autoimmunity.
Purpose of the Study:
- To investigate the plasticity of Th17 cells and the origin of IFN-γ-producing T cells during Th17 immunity.
- To understand the role of cytokines like IL-23 and IL-12 in modulating Th17 cell fate.
- To elucidate the developmental pathways influencing pathogenic potential of Th17 cells.
Main Methods:
- Development of IL-17F reporter mice to track cells committed to IL-17F and IL-17A expression.
- Analysis of Th17 cell differentiation and cytokine production under varying TGF-β conditions.
- Assessment of the roles of IL-23, IL-12, STAT4, and T-bet in regulating Th17 cell plasticity.
Main Results:
- Th17 cells require TGF-β for sustained expression of IL-17F and IL-17A.
- In the absence of TGF-β, IL-23 and IL-12 suppress IL-17 production and enhance IFN-γ production.
- This cytokine-driven plasticity is dependent on STAT4 and T-bet, key Th1 transcription factors.
- Distinct efficiencies were observed for IL-23 and IL-12 in driving this Th17 cell plasticity.
Conclusions:
- Th17 cell development exhibits late plasticity, allowing a switch in cytokine production.
- This plasticity is influenced by cytokine milieu (IL-23/IL-12) and STAT4/T-bet pathways in the absence of TGF-β.
- Understanding Th17 cell plasticity is crucial for developing strategies against autoimmune diseases and for enhancing host defense.
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