Sarcoidosis, a multisystem disorder, was previously defined by the presence of noncaseating epithelioid cell granuloma in affected organs following the exclusion of other known etiologic agents.1 Because of new immunologic data accumulated in the past 10 years,2,8 new criteria have been suggested for definition of sarcoidosis.4 Sarcoidosis should now be defined as a chronic, multisystem disorder characterized by an accumulation of inflammatory and immune effector cells,5,6 noncaseating granuloma, and derangement of normal tissue architecture in affected organs. Bronchoalveolar lavage (BAL), done in conjunction with fiberoptic bronchoscopy, was widely used in the early 1970s-a technique to recover for analysis of protein and cell contents from human lungs.7 Numerous studies8-47 about immunocompetent cells recovered by BAL from the lower respiratory tract of patients with Sarcoidosis have provided a better understanding of the immunologic events that take place at an important site of the disease-the respiratory tract. Although many organs can be affected by sarcoidosis, the lungs are most commonly involved (90%) and are the site of the disease that results in the highest morbidity and mortality,48 mostly because of severe functional impairment that occurs in the interstitial fibrosis stage of advanced disease. Therefore, this review will focus on pulmonary Sarcoidosis because this is a major site of involvement.20. Inflammation in the alveolar walls and air spaces, an initial host response to the disease process, causes an acute phase of mural and intraluminal alveolitis.49 Following perhaps the consequences of prolonged or smoldering inflammation, adjacent portions of the interstitium and vasculature can be involved by granulomas. At this step, the disease-host interaction may proceed in either of two ways: spontaneous regression or progress to fibrosis and scarring that replaces the normal lung tissue with fibroblasts and a collagenous matrix produced by these cells.
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