Sarcoidosis is a systemic inflammatory disorder that can potentially involve any part of the body, with a predilection for the lungs and intrathoracic lymph nodes (1). The histopathological hallmark of sarcoidosis is noncaseating granulomatous inflammation. The granulomas are typically discrete, compact organizations of epithelioid macrophages, T lymphocytes, monocytes, and fibroblasts. The granulomas are usually noncaseating, although fibrinoid necrosis may occasionally be present. Multinucleated giant cells, occasionally with inclusion bodies, are commonly formed within granulomas. The infiltration of organs by this inflammatory process leads to distortion of local architecture, tissue injury, with eventual deposition of ground substance, and fibrosis. Although the etiology of sarcoidosis remains unclear, the disease is thought to arise from an immune-mediated response to an antigenic stimulus that induces both innate and adaptive (antigen-specific) processes (2-4). These processes are regulated by key effector cytokines, as illustrated in experimental models of granuloma formation.
|Original language||English (US)|
|Title of host publication||Sarcoidosis|
|Number of pages||36|
|ISBN (Print)||0824759265, 9780824759261|
|State||Published - Jan 1 2005|
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