Abstract
This paper summarizes our research and the results obtained on the topic of immunology of interstitial lung disorders. Areas of investigation mainly included sarcoidosis, hypersensitivity pneumonitis (HP), and more recently the pulmonary involvement in acquired immunodeficiency syndrome (AIDS). In sarcoidosis patients two major mechanisms account for the alveolitis, i.e. an in situ cellular proliferation and a cellular redistribution from the peripheral blood to the sites of disease activity, including the lung. These findings involve both lymphocytes (CD4 helper-related cells) and macrophages, and lead to the formation and provide maintenance of sarcoid granuloma. In patients with hypersensitivity pneumonitis the lung infiltrates are characterized by cells bearing suppressor/cytotoxic phenotype. The expansion of cells with these characteristics in the lung of these patients is likely to be related to a local immune response to the antigenic stimulus. In the lung of patients with AIDS we also found a discrete lymphocytic alveolitis bearing the CD8 cytotoxic-related phenotype. The role of cytotoxic events, related to the lymphocytes and macrophages, which are operative in the lung of AIDS patients, is being evaluated. The analysis of cells recovered from the lavage, mainly lymphocytes and macrophages, in terms of surface phenotype, functional in vitro evaluations and molecular analysis, has provided new insights into the pathogenesis of the above quoted interstitial lung disorders.
Publisher
European Respiratory Society (ERS)
Subject
Pulmonary and Respiratory Medicine
Cited by
3 articles.
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