Immunological/physiological relationships in asthma: potential regulation by lung macrophages.
There is now a consensus that T-cell-mediated inflammation and eosinophil activation in the bronchial wall contribute to the pathogenesis of asthma. However, the relationship between these immunopathological mechanisms and the observed physiological aberrations remain unclear. Here, Len Poulter and colleagues identify the links between T-cell-mediated inflammation and bronchial hyperresponsiveness, and propose a hypothesis for asthma pathogenesis in which the combination of immunological and physiological abnormalities may result in the promotion of disease. Furthermore, they suggest that an integral factor in the prevention of this process is the regulation of bronchial T-cell reactivity by a population of immunosuppressive macrophages.
Poulter
L W
LW
Dept of Clinical Immunology, Royal Free Hospital School of Medicine, London, UK.
Janossy
G
G
Power
C
C
Sreenan
S
S
Burke
C
C
D001249:Asthma / Q000276:immunology / Q000503:physiopathology*; D016535:Bronchial Hyperreactivity / Q000276:immunology; D004804:Eosinophils / Q000276:immunology; D006801:Humans; D008168:Lung / Q000473:pathology / Q000503:physiopathology*; D008264:Macrophages / Q000502:physiology*; D013601:T-Lymphocytes / Q000276:immunology