By a News Reporter-Staff News Editor at Cancer Vaccine Week -- Investigators publish new report on Biotechnology. According to news reporting originating from Durham, North Carolina, by NewsRx correspondents, research stated, "Cancers subvert the host immune system to facilitate disease progression. These evolved immunosuppressive mechanisms are also implicated in circumventing immunotherapeutic strategies."
Our news editors obtained a quote from the research from Duke University, "Emerging data indicate that local tumor-associated DC populations exhibit tolerogenic features by promoting Treg development; however, the mechanisms by which tumors manipulate DC and Treg function in the tumor microenvironment remain unclear. Type III TGF-beta receptor (TGFBR3) and its shed extracellular domain (sTGFBR3) regulate TGF-beta signaling and maintain epithelial homeostasis, with loss of TGFBR3 expression promoting progression early in breast cancer development. Using murine models of breast cancer and melanoma, we elucidated a tumor immunoevasion mechanism whereby loss of tumor-expressed TGFBR3/sTGFBR3 enhanced TGF-beta signaling within locoregional DC populations and upregulated both the immunoregulatory enzyme indoleamine 2,3-dioxygenase (ID 0) in plasmacytoid. DCs and the CCL22 chemokine in myeloid DCs. Alterations in these DC populations mediated Treg infiltration and the suppression of antitumor immunity."
According to the news editors, the research concluded: "Our findings provide mechanistic support for using TGF-beta inhibitors to enhance the efficacy of tumor immunotherapy, indicate that sTGFBR3 levels could serve as a predictive immunotherapy biomarker, and expand the mechanisms by which TGFBR3 suppresses cancer progression to include effects on the tumor immune microenvironment."
For more information on this research see: Type III TGF-beta receptor downregulation generates an immunotolerant tumor microenvironment. Journal of Clinical Investigation, 2013;123(9):3925-3940. Journal of Clinical Investigation can be contacted at: Amer Soc Clinical Investigation Inc, 35 Research Dr, Ste 300, Ann Arbor, MI 48103, USA (see also technology.html">Biotechnology).
The news editors report that additional information may be obtained by contacting B.A. Hanks, Duke University, Medical Center, Dept. of Surg, Durham, NC 27708, United States. Additional authors for this research include A. Holtzhausen, K.S. Evans, R. Jamieson, P. Gimpel, O.M. Campbell, M. Hector-Greene, L.H. Sun, A. Tewari, A. George, M. Starr, A. Nixon, C. Augustine, G. Beasley, D.S. Tyler, T. Osada, M.A. Morse, L. Ling, H.K. Lyerly and Blob.
Keywords for this news article include: Biotechnology, Durham, Cancer, Oncology, United States, Immunotherapy, North Carolina, Immunomodulation, North and Central America
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