Regulation of lung inflammation in the model of IgG immune-complex injury.
Modern techniques of cell and molecular biology have rapidly uncovered the mechanisms underlying inflammatory injury of the lung. This expanding knowledge (which includes an understanding of complement, cell surface receptors, cytokines and chemokines, transcription factors, oxidants, proteinases, and endogenous inhibitors, as well as the role of leukocyte adhesion-promoting molecules) has provided new insights into the inflammatory system in general, as well as in the context of lung injury. In this review, we summarize recent progress in understanding the regulation of lung inflammation by using immunoglobulin G (IgG) immune complex-induced lung injury as a model. These studies have provided information on the role of various inflammatory mediators and their sequence of engagement. Insights into potential interventional approaches for the suppression of inflammatory processes in humans have emerged from those studies.
Gao
Hongwei
H
Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA. hgao@umich.edu
Neff
Thomas
T
Ward
Peter A
PA
D000542:Alveolitis, Extrinsic Allergic / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D000818:Animals; D000936:Antigen-Antibody Complex / Q000276:immunology* / Q000378:metabolism; D017209:Apoptosis / Q000276:immunology; D015415:Biomarkers / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology*
D000936:Antigen-Antibody Complex; D015415:Biomarkers; D007074:Immunoglobulin G