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In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse
Published on: October 25, 2024
IL-23 drives pathogenic IL-17-producing CD8+ T cells.
Bogoljub Ciric1, Mohamed El-behi, Rosalyn Cabrera
1Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA. bxc170@jefferson.edu
Journal of Immunology (Baltimore, Md. : 1950)
|April 22, 2009
Summary
CD8(+) T cells (Tc17) are involved in autoimmunity and cancer. IL-21 promotes Tc17 differentiation, and their pathogenicity in autoimmune diabetes depends on specific cytokine treatments.
Area of Science:
- Immunology
- Cell Biology
Background:
- IL-17-producing CD8(+) T cells (Tc17) are implicated in autoimmune diseases and cancer.
- Limited research exists on Tc17 cell biology and function.
Purpose of the Study:
- To elucidate the developmental characteristics and pathogenic potential of Tc17 cells.
- To investigate the role of cytokines like IL-21 and IL-23 in Tc17 cell differentiation and function.
Main Methods:
- Comparative analysis of Tc17 and Th17 cell development.
- Investigating the effects of IL-21, IL-23, TGF-beta1, and IL-6 on Tc17 cells.
- Assessing Tc17 cell pathogenicity in an autoimmune diabetes model.
Main Results:
- IL-21 promotes Tc17 cell differentiation; IL-23 drives IL-22 expression.
- STAT1 and STAT4 are crucial for Tc17 cell development and cytokine secretion.
- Tc17 cells can be pathogenic or nonpathogenic; IL-23-treated cells induce autoimmune diabetes, unlike those treated with TGF-beta1 plus IL-6.
Conclusions:
- Tc17 and Th17 cells share developmental pathways, with IL-21 being a novel promoter for Tc17 cells.
- The pathogenicity of Tc17 cells is context-dependent, influenced by cytokine milieu and their ability to recruit immune cells and initiate inflammation.
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