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Interference with intraepithelial TNF-α signaling inhibits CD8(+) T-cell-mediated lung injury in influenza infection.

Abstract：

:CD8(+) T-cell-mediated pulmonary immunopathology in respiratory virus infection is mediated in large part by antigen-specific TNF-α expression by antiviral effector T cells, which results in epithelial chemokine expression and inflammatory infiltration of the lung. To further define the signaling events leading to lung epithelial chemokine production in response to CD8(+) T-cell antigen recognition, we expressed the adenoviral 14.7K protein, a putative inhibitor of TNF-α signaling, in the distal lung epithelium, and analyzed the functional consequences. Distal airway epithelial expression of 14.7K resulted in a significant reduction in lung injury resulting from severe influenza pneumonia. In vitro analysis demonstrated a significant reduction in the expression of an important mediator of injury, CCL2, in response to CD8(+) T-cell recognition, or to TNF-α. The inhibitory effect of 14.7K on CCL2 expression resulted from attenuation of NF-κB activity, which was independent of Iκ-Bα degradation or nuclear translocation of the p65 subunit. Furthermore, epithelial 14.7K expression inhibited serine phosphorylation of Akt, GSK-3β, and the p65 subunit of NF-κB, as well as recruitment of NF-κB for DNA binding in vivo. These results provide insight into the mechanism of 14.7K inhibition of NF-κB activity, as well as further elucidate the mechanisms involved in the induction of T-cell-mediated immunopathology in respiratory virus infection.

journal_name

Viral Immunol

journal_title

Viral immunology

authors

Srikiatkhachorn A,Chintapalli J,Liu J,Jamaluddin M,Harrod KS,Whitsett JA,Enelow RI,Ramana CV

doi

10.1089/vim.2010.0076

subject

Has Abstract

pub_date

2010-12-01 00:00:00

pages

639-45

issue

6

eissn

0882-8245

issn

1557-8976

journal_volume

23

pub_type

杂志文章

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