In:
The Journal of Immunology, The American Association of Immunologists, Vol. 173, No. 2 ( 2004-07-15), p. 721-725
Abstract:
Respiratory virus infection results in considerable pulmonary immunopathology, a component of which results from the host immune responses. We have developed a murine model to specifically examine the lung injury due to CD8+ T cell recognition of an influenza hemagglutinin (HA) transgene on lung epithelium in the absence of replicating virus, after adoptive transfer. Lung injury is largely mediated by chemokines expressed by the epithelial cells upon T cell recognition mediated by TNF-α. To determine the critical source of TNF-α, HA-specific TNF−/− CD8+ T cells were transferred into HA transgenic animals, and lung injury was not observed, though these T cells exhibited no defect in antiviral activity in vivo. This indicates that the initiating event in the injury process is Ag-specific expression of TNF-α by antiviral CD8+ T cells upon recognition of alveolar epithelial Ag, and that the effector activities responsible for viral clearance may be dissociable from those resulting in immunopathology.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.173.2.721
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2004
detail.hit.zdb_id:
1475085-5
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