A Novel Pathway That Regulates Inflammatory Disease in the Respiratory Tract

In animals with acute airway inflammation followed by repeated exposure to inhaled Ag, inflammation wanes over time and thus limits the study of chronic airway inflammatory diseases such as asthma. We developed a model of airway inflammation and inhalational exposure to investigate regulatory pathwa...

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Bibliographic Details
Published in:Journal of Immunology 2007-03, Vol.178 (6), p.3846-3855
Main Authors: Niu, Naiqian, Le Goff, Marc K, Li, Fangyong, Rahman, Marina, Homer, Robert J, Cohn, Lauren
Format: Article
Language:English
Subjects:
Animals
Antigens - immunology
Asthma - immunology
Asthma - pathology
Asthma - therapy
Chronic Disease
Disease Models, Animal
Eosinophilia - immunology
Eosinophilia - pathology
Immune Tolerance
Inflammation - immunology
Inflammation - pathology
Inflammation - therapy
Macrophages - immunology
Macrophages - pathology
Mice
Mice, Inbred BALB C
Mice, Transgenic
Th1 Cells - immunology
Th1 Cells - pathology
Th2 Cells - immunology
Th2 Cells - pathology
Transforming Growth Factor beta1 - immunology
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Summary:In animals with acute airway inflammation followed by repeated exposure to inhaled Ag, inflammation wanes over time and thus limits the study of chronic airway inflammatory diseases such as asthma. We developed a model of airway inflammation and inhalational exposure to investigate regulatory pathways in the respiratory tract. We show that Th1- and Th2-induced airway inflammation followed by repeated exposure to inhaled Ag leads to a state of immunosuppression. Challenge of these animals with a marked population of TCR transgenic effector Th1 or Th2 cells results in a striking inhibition of inflammation and effector Th cells. In Th2 models, airway hyperresponsiveness, mucus, and eosinophilia are reduced. The inhibitory effects observed are Ag nonspecific, can be induced in lymphocyte-deficient mice, and are associated with a population of TGF-beta1-expressing macrophages. Induction of this pathway may offer potent localized treatment of chronic T cell-mediated respiratory illnesses and provide insights into the development of such diseases.
ISSN:0022-1767
1550-6606
1365-2567
DOI:10.4049/jimmunol.178.6.3846