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Developing the Epithelial, Viral, and Allergic Paradigm for Asthma*: Giles F. Filley Lecture

Michael J. Holtzman, MD, FCCP; Eugene Agapov, PhD; Edy Kim, AB; Joo-in Kim, MD; Jeffrey D. Morton, BSc
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*From the Department of Medicine, Division of Pulmonary and Critical Care Medicine, Washington University School of Medicine, St. Louis, MO.

Correspondence to: Michael J. Holtzman, MD, FCCP, Washington University School of Medicine, Campus Box 8052, 660 South Euclid Ave, St. Louis, MO 63110; e-mail: holtzmanm@msnotes.wustl.edu



Chest. 2003;123(3_suppl):377S-384S. doi:10.1378/chest.123.3_suppl.377S
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The concept that inflammation leads to hyperreactive and hypersecretory airway diseases (especially asthma and bronchitis) has led to a widening search for the types of inflammatory cells and mediators that are responsible for the cascade of events linking the initial stimulus to the final abnormality in airway function. Cell types implicated in the development of airway inflammation include immune cells as well as parenchymal cells. Cell-cell interactions are attributed to classes of mediators that include lipids, proteases, peptides, and cytokines. It is not yet possible to integrate all of this information into a single model for the development of airway inflammation, but a useful framework is based on the classification of the adaptive immune system, and especially the T-cell responses to allergic and nonallergic stimuli that enter the airway. This scheme was developed in murine models of the immune response in which CD4+ T-cell-dependent responses may be classified into T helper (Th) type 1 or Th2, in which Th1 cells characteristically mediate delayed-type hypersensitivity reactions and Th2 cells promote B-cell-dependent humoral immunity. In turn, the traditional scheme for asthma pathogenesis is based on a relative decrease in Th1 cellular responses in combination with an increase in Th2 responses (Fig 1 ).

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