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Type 1/Type 2 Cytokine Paradigm and the Progression of Pulmonary Fibrosis*

Nicholas W. Lukacs, PhD; Cory Hogaboam; Stephen W. Chensue, MD; Kate Blease; Steven L. Kunkel, PhD
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*From the Department of Pathology, University of Michigan Medical School, Ann Arbor, MI.

Correspondence to: Steven L. Kunkel, PhD, Professor, Department of Pathology, 1301 Catherine Rd, Box 0602, University of Michigan Medical School, Ann Arbor, MI 48109-0602; e-mail: slkunkel@umich.edu



Chest. 2001;120(1_suppl):S5-S8. doi:10.1378/chest.120.1_suppl.S5
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The pathogenesis of end-stage, chronic lung disease is thought to be characterized by an initial inflammatory response followed by fibroproliferation and deposition of extracellular matrix. Many of these chronic lung disorders share a variety of common properties, including an unknown etiology, undefined mechanisms of initiation and maintenance, and progressive fibrosis. Unfortunately, efficacious therapeutic options are not readily available for the treatment of many chronic lung diseases, which may reflect the limited scientific and mechanistic understanding of these disorders. However, recent studies have shown that cytokine networks are likely operative in dictating the progression of these diseases, as these mediators can influence fibroblast activation, proliferation, and collagen deposition during the maintenance of chronic fibrotic lung disease. Accumulating data support the concept that the specific cytokine phenotype may provide a fundamental mechanism for the regulation or continuation of the fibrotic process. For example, interferon-γ appears to suppresses fibroblast activities, such as proliferation and collagen production, while interleukin (IL)-4 and IL-13 can augment fibroblast growth and collagen production. Interestingly, these mediators are prototypic cytokines that functionally define either a type-1 or a type-2 immune response. Thus, experimental models of cell-mediated lung inflammation, which are characterized by either a type-1 or a type-2 response, will be useful in delineating the mechanisms that either maintain or resolve chronic lung inflammation and accompanying fibrosis.


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