• Media type: E-Article
  • Title: Immunosurveillance of Lung Melanoma Metastasis in EBI-3-Deficient Mice Mediated by CD8+ T Cells
  • Contributor: Sauer, Kerstin A.; Maxeiner, Joachim H.; Karwot, Roman; Scholtes, Petra; Lehr, Hans A.; Birkenbach, Mark; Blumberg, Richard S.; Finotto, Susetta
  • imprint: The American Association of Immunologists, 2008
  • Published in: The Journal of Immunology
  • Language: English
  • DOI: 10.4049/jimmunol.181.9.6148
  • ISSN: 0022-1767; 1550-6606
  • Keywords: Immunology ; Immunology and Allergy
  • Origination:
  • Footnote:
  • Description: <jats:title>Abstract</jats:title> <jats:p>EBV-induced gene 3 (EBI-3) codes for a soluble type I receptor homologous to the p40 subunit of IL-12 that is expressed by APCs following activation. In this study, we assessed the role of EBI-3 in a model of lung melanoma metastasis. Intravenous injection of the B16-F10 cell line resulted in a significant reduction of lung tumor metastasis in EBI-3−/− recipient mice compared with wild-type mice. The immunological finding accompanying this effect was the expansion of a newly described cell subset called IFN-γ producing killer dendritic cells associated with CD8+ T cell responses in the lung of EBI-3−/− mice including IFN-γ release and TNF-α-induced programmed tumor cell death. Depletion of CD8+ T cells as well as targeting T-bet abrogated the protective effects of EBI-3 deficiency on lung melanoma metastases. Finally, adoptive transfer of EBI-3−/− CD8+ T cells into tumor bearing wild-type mice inhibited lung metastasis in recipient mice. Taken together, these data demonstrate that targeting EBI-3 leads to a T-bet-mediated antitumor CD8+ T cell responses in the lung.</jats:p>
  • Access State: Open Access