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Global gene expression profiling in interleukin-12-induced activation of CD8(+) cytotoxic T lymphocytes against mouse mammary Carcinoma.

TitleGlobal gene expression profiling in interleukin-12-induced activation of CD8(+) cytotoxic T lymphocytes against mouse mammary Carcinoma.
Publication TypeJournal Article
Year of Publication2004
AuthorsCao S, Xiang Z, Ma X
JournalCell Mol Immunol
Volume1
Issue5
Pagination357-66
Date Published2004 Oct
ISSN1672-7681
KeywordsAdjuvants, Immunologic, Animals, Carcinoma, CD8-Positive T-Lymphocytes, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Immunity, Cellular, Interleukin-12, Lymphocyte Activation, Mammary Neoplasms, Experimental, Mice, Mice, Inbred BALB C, Neoplasm Transplantation, Oligonucleotide Array Sequence Analysis
Abstract

Interleukin-12 (IL-12) is a critical cytokine representing the link between the cellular and humoral branches of host immune defense apparatus. IL-12-induced cytotoxic lymphocyte (CTL) development is a central mechanism in immune responses against intracellular infectious agents as well as malignant growth. However, the molecular basis of tumor-specific CTL responses mediated by IL-12 remains poorly defined. In this study, we addressed this issue in a comprehensive manner to probe into IL-12-induced anti-tumor responses by global gene expression profiling of mRNA expression in CD8(+) T cells in a transplantable syngeneic mouse mammary carcinoma model treated or not with recombinant IL-12. A strong tumor regression was induced by the IL-12 treatment. An introspection of differential gene expression at an early stage of the IL-12-initiated CTL activation reveals interesting genes and molecular pathways that may account for the marked tumor regression, and is likely to provide a rich source of potential targets for further research and development of effective therapeutic modalities.

Alternate JournalCell Mol Immunol
PubMed ID16285895
PubMed Central IDPMC2965067
Grant ListR01 CA100223 / CA / NCI NIH HHS / United States
R01 CA100223-01A1 / CA / NCI NIH HHS / United States

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