Affiliation:
1. Department of Pediatrics, Division of Pulmonology, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania 15201;, ,
2. Department of Genetics, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112
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 TH17 was shown to play a role in regulating neutrophilic and macrophage inflammation in the lung, suggesting a potential role for TH17 cells in severe, steroid-insensitive asthma and COPD.
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308 articles.
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