The contribution of NKT cells, NK cells, and other γ-chain-dependent non-T non-B cells to IL-12-mediated rejection of tumors

Se-Ho Park, Tim Kyin, Albert Bendelac, Claude Carnaud

Research output: Contribution to journalArticle

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Abstract

IL-12 is a potent cytokine that impairs the growth of several tumors in vivo in natural as well as in therapeutic conditions. Although IL-12 can enhance a number of immunological antitumor mechanisms, including those mediated by NK cells and CTL, recent reports have suggested that the mouse CD1d-restricted Vα14-Jα18 NKT cell was the essential cell type recruited in most, if not all tumor rejection models, including the B16 melanoma. In this study, we have examined and compared the role of NKT cells, T cells, NK cells, and other non-T non-B cells in the rejection of B16 melanoma cells after exogenous administration of IL-12. Surprisingly, our results failed to confirm a necessary role for NKT cells in this model. Instead, we found that NK cells mediated the rejection of liver metastases, whereas other γc-dependent non-T non-B cells, possibly lymphoid dendritic cells, were required for rejection of skin tumors. These findings challenge the view that NKT cells are systematically required for IL-12-mediated rejection of tumors, and instead reveal that a variety of effector pathways can be recruited depending on the tumor microenvironment.

Original languageEnglish
Pages (from-to)1197-1201
Number of pages5
JournalJournal of Immunology
Volume170
Issue number3
Publication statusPublished - 2003 Feb 1

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Natural Killer T-Cells
Interleukin-12
Natural Killer Cells
Experimental Melanomas
Neoplasms
Tumor Microenvironment
Dendritic Cells
Lymphocytes
Cytokines
Neoplasm Metastasis
T-Lymphocytes
Skin
Liver
Growth
Therapeutics

ASJC Scopus subject areas

  • Immunology

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The contribution of NKT cells, NK cells, and other γ-chain-dependent non-T non-B cells to IL-12-mediated rejection of tumors. / Park, Se-Ho; Kyin, Tim; Bendelac, Albert; Carnaud, Claude.

In: Journal of Immunology, Vol. 170, No. 3, 01.02.2003, p. 1197-1201.

Research output: Contribution to journalArticle

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