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Immune Dysfunction in Patients with Chronic Obstructive Pulmonary Disease.

Tariq A Bhat¹, Louis Panzica¹, Suresh Gopi Kalathil¹

¹Department of Immunology, Roswell Park Cancer Institute, Buffalo, New York.

Annals of the American Thoracic Society

|November 24, 2015

Summary

Chronic obstructive pulmonary disease (COPD) involves chronic lung inflammation. Immune dysfunction in COPD patients worsens disease severity and respiratory infections, suggesting therapeutic targets.

Keywords:

COPD adaptive immunity immune dysfunction innate immunity

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Area of Science:

Pulmonary Medicine
Immunology
Respiratory Diseases

Background:

Chronic obstructive pulmonary disease (COPD) is characterized by chronic lung inflammation, significantly influenced by cigarette smoke (CS).
CS exposure triggers inflammatory responses, recruiting immune cells and establishing a chronic inflammatory microenvironment.
This chronic inflammation leads to lung damage, impaired immunity, and recurrent respiratory infections, exacerbating COPD pathology.

Purpose of the Study:

To review the role of immune dysfunction in the pathogenesis of COPD.
To explore how immune dysfunction contributes to recurrent respiratory infections and disease severity in COPD.
To discuss potential therapeutic strategies targeting immunosuppressive networks in COPD.

Main Methods:

Review of existing literature on COPD pathogenesis, inflammation, and immune responses.
Analysis of studies investigating the effects of CS on lung inflammation and immunity.
Examination of immune cell phenotypes in COPD patients compared to healthy controls.

Main Results:

CS exposure exacerbates lung inflammation and compromises immunity to respiratory pathogens in a mouse model of COPD.
COPD patients exhibit immune dysfunction, characterized by T regulatory cells, exhausted effector T cells, and myeloid-derived suppressor cells.
These findings highlight the contribution of specific immune cell populations to disease severity and susceptibility to infections.

Conclusions:

Immune dysfunction is a critical factor in COPD, contributing to disease severity and recurrent infections.
Targeting immunosuppressive networks, such as regulatory T cells and myeloid-derived suppressor cells, presents a promising therapeutic strategy.
Restoring functional immune responses could improve lung function and reduce exacerbations in COPD patients.