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Alveolar Epithelial Cell Chemokine Expression Induced by Specific Antiviral CD8+ T-Cell Recognition Plays a Critical Role in the Perpetuation of Experimental Interstitial Pneumonia*

Min Q. Zhao, MD, PhD; Maura P. Foley, MD; Mark H. Stoler, MD; Richard I. Enelow, MD
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*From the University of Virginia Health Sciences Center, Charlottesville, VA.

Correspondence to: Richard I. Enelow, MD, Department of Medicine, University of Virginia Health System, Box 546, Charlottesville, VA 22908; email: enelow@virginia.edu



Chest. 2001;120(1_suppl):S11-S13. doi:10.1378/chest.120.1_suppl.S11
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CD 8+ T cells infiltrate the lung in a variety of inflammatory and interstitial lung diseases, though little is known about the functional activities expressed by these cells in the lung parenchyma.13 The function of CD8+ T cells in viral defense is likely mediated by several effector activities, including cytotoxicity and cytokine secretion, but it is unclear to what extent these activities participate in injury associated with disease. CD8+ T-cell clearance of experimental respiratory virus infection results in considerable lung injury,4 though it is difficult to distinguish the deleterious effects of T-cell–effector activity from those of the virus infection itself. We have developed a murine model for the purpose of studying the direct effects of CD8+ T-cell recognition of antigens presented by alveolar epithelial cells, in the absence of virus infection. The model antigen is the A/Japan/57 influenza hemagglutinin, expressed under the transcriptional control of the surfactant protein C (SP-C) promoter, resulting in alveolar epithelial expression. Adoptive transfer of CD8+ T cells activated against hemagglutinin into these mice results in severe interstitial pneumonitis and significant lung injury, characterized by restrictive respiratory mechanics and significant diminution in carbon monoxide diffusing capacity.5 The functional deficits correlate more closely with the host inflammatory influx than with the initial T-cell infiltration. We have previously shown that neither perforin nor Fas is necessary for lung injury triggered by CD8+ T-cell transfer, but that tumor necrosis factor (TNF)-α is essential.6

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