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Emerging Mechanisms of Immunosuppression in Oral Cancers

¹ The Jane and Jerry Weintraub Center for Reconstructive Biotechnology, and Division of Oral Biology and Medicine, Jonsson Comprehensive Cancer Center (JCCC),
² Department of Head and Neck surgery, and
³ Department of Radiation Oncology, UCLA School of Dentistry and Medicine, 10833 Le Conte Ave., University of California, Los Angeles, CA 90095-1668, USA

View larger version (25K): [in this window] [in a new window]   Figure 1. Hypothetical representation of the steps involved in recruitment, activation, and expansion of NK cells by HEp2- I B(S32AS36A) cells. NFB knock-down HEp2 tumor cells, by producing large amounts of chemokines MCP-1 and RANTES, recruit NK cells. Due to a decrease in inhibitory signals—provided, for instance, by inhibitory MHC Class I antigens, IL-6 cytokine, and VEGF—NK cells remain viable and increase their functional activation at the site of pathology. Increased survival, in addition to augmented proliferation, results in significant expansion of the NK cells.

View larger version (25K): [in this window] [in a new window]   Figure 2. Cytokines and growth factors produced by tumor cells impair host anti-tumor immunity by activating STAT3 signaling in both tumor cells and professional antigen-presenting cells. Tumor cells expressing constitutively active NFB and STAT3 produce greatly reduced levels of RANTES and IP-10, thereby impairing T-cell infiltration and migration to the sites of tumor growth. In addition, several tumor-derived cytokines and growth factors activate STAT3 in immature dendritic cells, which blocks DC differentiation and expression of co-stimulatory molecules such as CD80 and CD86. High levels of immature DCs (iDC) can actively induce T-cell tolerance to tumor antigens and promote cancer progression.

Journal of Dental Research, Vol. 85, No. 12, 1061-1073 (2006)
DOI: 10.1177/154405910608501201


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