{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T09:07:03Z","timestamp":1778663223006,"version":"3.51.4"},"reference-count":46,"publisher":"SAGE Publications","issue":"6","license":[{"start":{"date-parts":[[2010,12,1]],"date-time":"2010-12-01T00:00:00Z","timestamp":1291161600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Viral Immunology"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:p>\n                    CD8\n                    <jats:sup>+<\/jats:sup>\n                    T-cell-mediated pulmonary immunopathology in respiratory virus infection is mediated in large part by antigen-specific TNF-\u03b1 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\n                    <jats:sup>+<\/jats:sup>\n                    T-cell antigen recognition, we expressed the adenoviral 14.7K protein, a putative inhibitor of TNF-\u03b1 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.\n                    <jats:italic toggle=\"yes\">In vitro<\/jats:italic>\n                    analysis demonstrated a significant reduction in the expression of an important mediator of injury, CCL2, in response to CD8\n                    <jats:sup>+<\/jats:sup>\n                    T-cell recognition, or to TNF-\u03b1. The inhibitory effect of 14.7K on CCL2 expression resulted from attenuation of NF-\u03baB activity, which was independent of I\u03ba-B\u03b1 degradation or nuclear translocation of the p65 subunit. Furthermore, epithelial 14.7K expression inhibited serine phosphorylation of Akt, GSK-3\u03b2, and the p65 subunit of NF-\u03baB, as well as recruitment of NF-\u03baB for DNA binding\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    . These results provide insight into the mechanism of 14.7K inhibition of NF-\u03baB activity, as well as further elucidate the mechanisms involved in the induction of T-cell-mediated immunopathology in respiratory virus infection.\n                  <\/jats:p>","DOI":"10.1089\/vim.2010.0076","type":"journal-article","created":{"date-parts":[[2010,12,8]],"date-time":"2010-12-08T12:38:25Z","timestamp":1291811905000},"page":"639-645","source":"Crossref","is-referenced-by-count":23,"title":["Interference with Intraepithelial TNF-\u03b1 Signaling Inhibits CD8\n                    <sup>+<\/sup>\n                    T-Cell-Mediated Lung Injury in Influenza Infection"],"prefix":"10.1177","volume":"23","author":[{"given":"Anon","family":"Srikiatkhachorn","sequence":"first","affiliation":[{"name":"University of Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jyothi","family":"Chintapalli","sequence":"additional","affiliation":[{"name":"Yale University School of 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