Chest
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via ISI Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lukacs, N. W.
Right arrow Articles by Kunkel, S. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lukacs, N. W.
Right arrow Articles by Kunkel, S. L.
(Chest. 2001;120:S5-S8.)
© 2001 American College of Chest Physicians

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

Nicholas W. Lukacs, PhD; Cory Hogaboam; Stephen W. Chensue, MD; Kate Blease and Steven L. Kunkel, PhD

* 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{at}umich.edu

Abstract

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-{gamma} 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.

Key Words: chemoattractant protein • chemokines • cytokines • experimental models • fibrosis • interferon-{gamma} • interleukin-4 • interleukin-12 • interleukin-13 • monocyte chemoattractant protein






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2001 by the American College of Chest Physicians.