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Updated: Jun 17, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
T helper 17 cells: discovery, function, and physiological trigger
Miriam Beer Torchinsky1, J Magarian Blander
1Department of Medicine, Immunology Institute, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, NY 10029, USA.
T helper 17 (T(H)17) cells are crucial for fighting infections and causing autoimmune inflammation. Their differentiation is triggered by recognizing apoptotic cells during infection, offering new insights into adaptive immunity.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- T helper 17 (T(H)17) cells are key players in host defense and autoimmune inflammation.
- These cells secrete various cytokines, including IL-17, IL-21, IL-10, and IL-22, influencing multiple tissues.
- T(H)17 differentiation requires TGF-beta and IL-6, highlighting its connection with FOXP3(+) regulatory T cells.
Purpose of the Study:
- To review current knowledge on T(H)17 cell effector functions and differentiation pathways.
- To discuss the physiological stimulus for T(H)17 cell development.
- To provide a framework for understanding effector T cell differentiation and CD4(+) T cell adaptive immunity.
Main Methods:
- Literature review and synthesis of existing research on T(H)17 cells.
- Discussion of cytokine profiles and differentiation requirements.
- Analysis of the role of apoptosis recognition in T(H)17 development.
Main Results:
- T(H)17 cells possess broad effector functions due to their diverse cytokine production.
- Distinct differentiation requirements link T(H)17 cells with regulatory T cells.
- Innate immune recognition of apoptotic cells during infection is a physiological trigger for T(H)17 differentiation.
Conclusions:
- Understanding T(H)17 cell biology is essential for both host defense and autoimmune disease research.
- The discovery of a specific physiological stimulus refines our understanding of T(H)17 development.
- This growing knowledge advances the framework for adaptive immune responses mediated by CD4(+) T cells.
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