Lymphocyte subsets in experimental bronchopulmonary inflammation and hyperresponsiveness

• Published in: Research in immunology (Paris) 1997, Vol.148 (1), p.13-18
• Main Authors: Coyle, A.J., Kopf, M.
• Format: Article
• Language: English
• Subjects: Animals; Bronchitis - immunology; Humans; Interferon-gamma - pharmacology; Interleukin-12 - pharmacology; Interleukin-5 - physiology; Lymphocyte Activation; Lymphocyte Subsets - immunology; Pneumonia - immunology
• ISSN: 0923-2494
• DOI: 10.1016/S0923-2494(97)86269-4

Exaggerated airway responsiveness to both specific stimuli (such as allergens in allergic individuals) and non-specific stimuli (such as cholinergic agonists, cold air, etc) is a characteristic feature of bronchial asthma. While the mechanisms underlying this bronchial hyperresponsiveness are still unclear, there is a considerable body of evidence to suggest that inflammation of the airway mucosa is of central importance. The most common pathological finding in the airways is that of an increase in the number of eosinophils and mast cells. In addition, ultrastructural abnormalities in the architecture of the lungs of asthmatic individuals have been reported, and are characterized by subepithelial deposition of collagen types III and V together with increased production of fibronectin. Eosinophil accumulation and activation, with the subsequent release of cationic proteins such as major basic protein (MBP), have been implicated in many of these pathological changes and subsequent modifications in airway function, although this still remains an area of intense discussion. The precise mechanisms by which these cells infiltrate the airways remain to be fully elucidated, although evidence is accumulating to suggest that soluble factors derived principally from T cells play a pivotal role in orchestrating this inflammatory response of the lungs. Here we discuss the various T-cell subsets and cytokine networks that exist in the allergic lung that may play an important role in the induction and maintenance of lung inflammation and changes in airway responsiveness.