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Updated: Jul 17, 2026

Isolation and Th17 Differentiation of Na&iuml;ve CD4 T Lymphocytes
12:59

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Published on: September 26, 2013

Autoimmune inflammation from the Th17 perspective.

Janette Furuzawa-Carballeda1, María Inés Vargas-Rojas, Antonio R Cabral

  • 1Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Vasco de Quiroga 15 Tlalpan, Mexico City 14000, Mexico.

Autoimmunity Reviews
|February 10, 2007
PubMed
Summary

The study identifies a distinct CD4+ T cell subset, Th17, crucial for autoimmune diseases like rheumatoid arthritis. Targeting the IL-17/23 pathway shows promise for treating these inflammatory conditions.

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Area of Science:

  • Immunology
  • Cell Biology
  • Autoimmunity

Background:

  • A distinct pro-inflammatory CD4+ T cell lineage, Th17, characterized by IL-17 production, has been identified.
  • Th17 cells differ from Th1 and Th2 cells and play a significant role in autoimmune pathogenesis.

Purpose of the Study:

  • To elucidate the role of Th17 cells and the IL-23 cytokine in the development of autoimmune diseases.
  • To investigate the differentiation factors and regulatory mechanisms governing Th17 cell development.
  • To explore the therapeutic potential of targeting the IL-17/23 axis in autoimmune conditions.

Main Methods:

  • Gene-targeted mouse models (IL-23 and IL-12 knockout) were used to study experimental autoimmune encephalomyelitis (EAE) and collagen-induced arthritis (CIA).
  • Analysis of T cell populations, including IL-17-producing CD4+ T cells and IFN-gamma-producing Th1 cells, in disease models.
  • Investigation of cytokines (TGF-beta, IL-6, IL-1, IL-23, IL-27) and transcription factors (RORgammat) involved in Th17 differentiation and function.

Main Results:

  • Mice lacking IL-23 (p19-/-) were resistant to EAE and CIA, correlating with a lack of IL-17-producing CD4+ T cells.
  • IL-12 knockout mice (p35-/-) showed strong development of both autoimmune diseases, despite the presence of Th1 cells.
  • Transforming growth factor-beta (TGF-beta), IL-6, and IL-1 were identified as key differentiation factors for Th17 cells, while IL-23 is essential for their expansion and survival.
  • IL-27 was found to potently inhibit Th17 development, and RORgammat was identified as the master regulator of Th17 differentiation.

Conclusions:

  • The IL-17/23 axis is critical for the pathogenesis of autoimmune diseases such as rheumatoid arthritis and multiple sclerosis.
  • IL-23 plays a crucial role in the expansion and survival of Th17 cells, contributing to autoimmune inflammation.
  • Targeting the IL-17/23 pathway represents a promising therapeutic strategy for managing IL-17-mediated autoimmune diseases.