Abstract

Studies of Molecular Mechanisms in Tuberculosis (7) Dendritic cells are the most potent antigen-presenting cells, and Epidemiology of Tuberculosis (7) they play a central role in initiating the primary immune reDiagnosis of Tuberculosis (1) sponse. To study their role in granulomatous inflammation, Treatment of Tuberculosis (5) Tsuchiya and coworkers (1) studied pulmonary granulomas elicNontuberculous Lung Infection (12) ited by Bacillus Calmette-Guerin (BCG) in rats. At the borders Human Immunodeficiency Virus Infection (2) of the pulmonary granulomas, numerous large, pleiomorphic Highly Active Antiretroviral Therapy (2) cells stained positive for OX62, an antibody specific for dendritic Lung Infections (10) cells. Ultrastructural morphology was characteristic of dendritic Host Defenses (5) cells. The cells showed intense surface expression of major histoPneumonia (3) compatibility complex class II, B7–1 and B7–2, and the absence Antimicrobial Therapy (2) of T cell markers and monocyte/macrophage-specific markers. Interstitial Lung Disease (39) The cells produced potent stimulation of allogenic T cells and Idiopathic Pulmonary Fibrosis (14) syngeneic T cells specific for purified protein derivative in the Genetics (2) absence of exogenous peptides. The authors conclude that denHistopathological Subtypes (1) dritic cells participate in the formation of pulmonary granulomas Serum Markers (1) elicited by BCG in rats, suggesting that dendritic cells play a Clinical Assessment (2) pivotal role in T cell–mediated granulomatous immune reCellular and Molecular Mechanisms, in vivo (3) sponses. An editorial commentary by Dreher and Nicod (2) Cellular and Molecular Mechanisms, ex vivo (1) accompanies this article. Animal Models (1) Although nitric oxide may contribute to host defense against Treatment (1) tuberculosis, its expression in human tuberculous lungs has not Statements and Workshops (2) been systematically characterized. In surgically resected lungs Progressive Systemic Sclerosis (3) of eight patients with tuberculosis, Choi and coworkers (3) found Sarcoidosis (3) increased levels of inducible nitric oxide synthase, endothelial Genetics (2) nitric oxide synthase, and nitrotyrosine (a marker of nitric oxide Molecular Mechanisms (1) expression) in the inflammatory zone of tuberculous granulomas Histiocytosis X (2) and in the nongranulomatous pneumonitis zone; the level of Lymphangioleiomyomatosis (2) neuronal nitric oxide synthase was not elevated. Tumor necrosis Eosinophilic Pneumonia (3) factorwas increased and principally localized to the necrotic Acute Interstitial Pneumonitis (2) areas of granulomas, and localized to a lesser degree in the Niemann-Pick Disease (1) inflammatory and fibrotic areas. The nitric oxide isoforms and Lymphoproliferative Disorders (1) tumor necrosis factorwere expressed by the epithelioid macroIdiopathic Pulmonary Alveolar Proteinosis (1) phages and giant cells within the granulomas and in alveolar Pulmonary Drug Toxicity (2) macrophages and epithelial cells in areas of pneumonitis. The Calcium Deposition in the Lung (1) authors conclude that nitric oxide and isoenzymes of nitric oxide Rodent Model of Bleomycin Fibrosis (4) synthase are present in specialized areas of tuberculous granuloOccupational Lung Disease (12) mas. An editorial commentary by Nathan (4) accompanies this Social Issues, Health Policy, Economics, and Journalology (6) article. Journalology (6) Because CD8 T cells play an important role in host defense

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