Abstract
Sarcoidosis can involve any tissue or organ. However, the finding that 90% of patients have lesions in the lungs, thoracic lymph nodes, or both provides evidence that the disease probably begins in the respiratory tract and the associated lymphatic system. Pulmonary sarcoidosis begins as an alveolitis or an accumulation of inflammatory cells within the alveolus. Large numbers of lymphocytes are present within the alveolar interstitium and on alveolar surfaces. In active pulmonary sarcoidosis, activated T lymphocytes spontaneously produce a number of factors in addition to interleukin-2 that are important in the development and maintenance of the inflammatory process: macrophage chemotactic factor, leukocyte inhibitoryfactor, γ-interferon, but not interleukin-1. The macrophages in granulomas are derived from monocytes that originate in the bone marrow and reach the site of inflammation by way of the peripheral circulation. Enhanced antibody production by pulmonary B-cells in sarcoid lesions apparently accounts for hypergammaglobulinemia that commonly occurs in the disease.
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