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Related Experiment Video

Updated: Jul 2, 2026

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Published on: April 16, 2019

Th17 cells in airway diseases.

Suzanne L Traves¹, Louise E Donnelly

¹Department of Physiology and Biophysics, Airways Inflammation Group, Institute of Infection, Immunity and Inflammation, Faculty of Medicine, University of Calgary, Alberta, Canada.

Current Molecular Medicine

|August 12, 2008

Summary

New research identifies T helper 17 (Th17) cells as key players in airway inflammation. These cells may drive neutrophilic inflammation in asthma and COPD, offering potential new therapeutic targets.

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Last Updated: Jul 2, 2026

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

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Published on: April 16, 2019

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Published on: October 25, 2024

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

Area of Science:

Immunology
Respiratory Medicine

Background:

Chronic inflammation characterizes many airway diseases like asthma and COPD.
Leukocyte accumulation in the lungs contributes to disease pathophysiology.
T helper 17 (Th17) cells, a distinct CD4+ lymphocyte subset, have been identified.

Purpose of the Study:

To explore the role of Th17 cells in airway inflammation.
To investigate the potential contribution of Th17 cells to asthma and COPD pathogenesis.

Main Methods:

Review of existing literature on Th17 cell differentiation and function.
Analysis of cytokine profiles and transcription factor expression (RORgammat).
Examination of IL-17 expression in asthma and COPD.

Main Results:

Th17 cell differentiation requires TGF-beta and IL-6, and is inhibited by IFN-gamma and IL-4.
IL-17, a key cytokine produced by Th17 cells, up-regulates neutrophil-attracting chemokines (CXCL1, CXCL6, CXCL8) and survival factors (GM-CSF, G-CSF).
IL-17 can potentiate inflammatory responses synergistically with other mediators.

Conclusions:

Th17 cells are implicated in promoting and sustaining neutrophilic inflammation in severe asthma and COPD.
The presence of Th17 cells in airways requires confirmation.
Th17 cells represent a potential novel therapeutic target for reducing lung neutrophilic inflammation.