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Updated: Jun 6, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

IL-17 and Th17 cells in tuberculosis.

Egídio Torrado¹, Andrea M Cooper

¹Trudeau Institute, Inc., 154 Algonquin Ave., Saranac Lake, NY 12983, USA.

Cytokine & Growth Factor Reviews

|November 16, 2010

Summary

Tuberculosis control requires balancing immune responses in the lungs. Regulating interferon-gamma (IFN-γ) and interleukin-17 (IL-17) is crucial to fight Mycobacterium tuberculosis and prevent tissue damage.

Area of Science:

Immunology
Infectious Diseases
Pulmonology

Background:

Tuberculosis (TB) primarily affects the lungs, necessitating continuous cellular immunity to control Mycobacterium tuberculosis.
Chronic inflammation and pathology can arise from persistent immune responses in the lung.
Both IFN-γ and IL-17 are induced during primary TB, driving inflammation and granuloma formation.

Purpose of the Study:

To investigate the critical role of immune response regulation in tuberculosis.
To understand the balance between Th1 (IFN-γ) and Th17 (IL-17) responses in controlling Mycobacterium tuberculosis and preventing immunopathology.

Main Methods:

This study focuses on the immunological mechanisms during tuberculosis infection.
Analysis of cytokine profiles, specifically Interferon-gamma (IFN-γ) and Interleukin-17 (IL-17), in the context of Mycobacterium tuberculosis infection.

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Main Results:

During primary TB, both IFN-γ and IL-17 are induced, promoting inflammation and granuloma organization.
A balance between Th1 and Th17 responses is essential during chronic TB to control bacterial growth and limit tissue damage.
Excessive IL-17 production can lead to neutrophil recruitment and significant tissue damage.

Conclusions:

Regulation of Th1 and Th17 immune responses is vital for effective anti-mycobacterial immunity.
Maintaining a balance between these T-helper cell responses is key to preventing severe immunopathological consequences in tuberculosis.
Immune modulation strategies targeting Th1/Th17 balance may offer therapeutic potential for TB.