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Updated: Jun 8, 2026
12:59
Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
[Cytokines and T cell differentiation in systemic sclerosis]
1Service de médecine interne, CHU Ambroise-Paré, Assistance publique-Hôpitaux de Paris, 9, avenue Charles-de-Gaulle, 92100 Boulogne-Billancourt, France. salim.trad@apr.aphp.fr
La Revue De Medecine Interne
|September 21, 2010
Summary
Systemic sclerosis involves complex interactions, but T cell differentiation, particularly Th17, Th22, and regulatory T cells (Treg), is crucial. An imbalance, with Th22 overexpression and Treg underactivity, may drive inflammation in this autoimmune disease.
Area of Science:
- Immunology
- Autoimmune Diseases
- Cell Biology
Context:
- Systemic sclerosis (SSc) pathophysiology involves complex interactions: vasculopathy, inflammation, fibrosis, and autoimmunity.
- The precise interplay between vascular disease and inflammatory cell infiltration in SSc remains unclear.
- T cell activation and cytokine expression are implicated in vascular damage and collagen dysregulation in SSc.
Purpose:
- To create a comprehensive map of cytokines influencing T cell differentiation pathways.
- To review recent advancements in T lymphocyte differentiation, including Th9, Th17, Th22, and regulatory T cells (Treg).
- To focus on Th17, Th22, and Treg differentiation in the context of inflammation-tolerance balance.
Summary:
- T cell involvement in SSc appears as a Th1/Th2 co-expression rather than exclusive polarization.
- Evidence suggests a potential imbalance between Th22 and Treg cells in SSc.
- This imbalance may involve Th22 cell overexpression, contributing to tissue inflammation in SSc.
Impact:
- Provides a detailed overview of cytokines regulating T cell differentiation in SSc.
- Highlights the potential role of Th22/Treg imbalance in SSc pathogenesis.
- Offers insights into novel therapeutic targets for managing SSc-related inflammation and fibrosis.
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