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Dept of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan Medical Center, Ann Arbor, Michigan, USA
CORRESPONDENCE: G.B. Toews, University of Michigan School of Medicine, 6301 MSRB III, 1150 W. Medical Center Drive, Ann Arbor, MI 48109-0642, USA. Fax: 1 7347644556
Keywords: Antibodies, immunology, lymphocytes, pulmonary host defences
Received: March 22, 2001
Accepted May 8, 2001
This research was supported in part by a Research Grant from the American Lung Association and a Parker B. Francis Fellowship Award (T.A. Moore) and grants CA79046 (B.B. Moore), HL51082 (G.B. Toews), P50HL56402 (G.B. Toews and B.B. Moore), and HL60289 (G.B. Toews, B.B. Moore and T.A. Moore) from the National Institutes of Health. In addition, G.B. Toews is supported by a Merit Review grant from the Veteran's Administration.
Abstract
Pulmonary infectious diseases cause significant morbidity and mortality in both industrialized and developing countries.
Adaptive immune responses are required to defend the lung against pathogens that survive in normal macrophages and extracellular organisms that evade phagocytosis. Microbes initiate both innate immune responses and specific adaptive immune responses.
Innate immune response molecules regulate T-;lymphocyte differentiation. Activated T-;lymphocytes provide cytokines, which activate macrophages and lytic signals that lyse infected antigen-presenting cells.
Antibodies produced by plasma cells facilitate microbial clearance through diverse effector mechanisms including opsonization, complement fixation and antibody-dependent cytotoxicity. Lymphocytes determine the specificity of the immune response and orchestrate effector limbs of the immune response.
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