TH17 cells in asthma and COPD

Annu Rev Physiol. 2010;72:495-516. doi: 10.1146/annurev-physiol-021909-135926.

Abstract

Asthma and chronic obstructive pulmonary disease (COPD) represent two classes of chronic obstructive lung disorders that may share some similar immunologic mechanisms of disease. Asthma is a complex human disease characterized by airway hyperresponsiveness (AHR) and inflammation, whereas COPD is marked by progressive emphysematic changes in the lung. Recently it has been shown that advanced COPD is characterized by lymphoid follicles, drawing attention to immunological mechanisms in COPD. Despite numerous studies in mice to elucidate the immunologic mechanisms of asthma, sufficient current treatment options are limited. Clinically, many asthma patients fail to satisfactorily respond to standard steroid therapy, and this type of steroid-resistant, severe asthma has been linked to the presence of neutrophilic inflammation in the lung. The role of neutrophils, macrophages, and their secreted proteases in COPD needs to be better defined. Recently, the T lymphocyte subset T(H)17 was shown to play a role in regulating neutrophilic and macrophage inflammation in the lung, suggesting a potential role for T(H)17 cells in severe, steroid-insensitive asthma and COPD.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / therapeutic use
  • Asthma / drug therapy
  • Asthma / metabolism
  • Asthma / pathology*
  • Drug Resistance
  • Humans
  • Inflammation / pathology
  • Interleukin-17 / metabolism
  • Interleukin-17 / physiology*
  • Lung / pathology
  • Neutrophils / pathology
  • Pulmonary Disease, Chronic Obstructive / metabolism
  • Pulmonary Disease, Chronic Obstructive / pathology*
  • Receptors, Interleukin-17 / metabolism
  • Receptors, Interleukin-17 / physiology
  • Signal Transduction / physiology
  • Steroids / therapeutic use
  • T-Lymphocyte Subsets / metabolism
  • T-Lymphocyte Subsets / pathology*

Substances

  • Anti-Inflammatory Agents
  • Interleukin-17
  • Receptors, Interleukin-17
  • Steroids