ABSTRACT
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 nonca-
seating granulomatous inflammation. The granulomas are typically discrete,
compact organizations of epithelioid macrophages, T lymphocytes, mono-
cytes, 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 granulo-
mas. The infiltration of organs by this inflammatory process leads to distor-
tion 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-spe-
cific) processes (2-4). These processes are regulated by key effector cyto-
kines, as illustrated in experimental models of granuloma formation.
