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Intratumoral Injection of CpG Oligonucleotides Induces the Differentiation and Reduces the Immunosuppressive Activity of Myeloid-Derived Suppressor Cells

  1. Author:
    Shirota, Y.
    Shirota, H.
    Klinman, D. M.

  2. Author Address

    [Shirota, Yuko; Shirota, Hidekazu; Klinman, Dennis M.] NCI, Canc & Inflammat Program, Frederick, MD 21702 USA. [Shirota, Hidekazu] NCI, Basic Sci Program, Sci Applicat Int Corp Frederick, Frederick, MD 21703 USA.;Klinman, DM (reprint author), NCI, Canc & Inflammat Program, Bldg 567,Room 205, Frederick, MD 21702 USA;klinmand@mail.nih.gov
    1. Year: 2012
    2. Date: Feb
  2. Journal: Journal of Immunology
    1. 188
    2. 4
    3. Pages: 1592-1599
  4. Type of Article: Article
  5. ISSN: 0022-1767
  1. Abstract:

    Immunostimulatory CpG oligonucleotides (ODN) activate cells that express TLR9 and have been shown to improve the host's response to tumor Ags. Unfortunately, the immunosuppressive microenvironment that surrounds many cancers inhibits Ag-specific cellular responses and thus interferes with CpG-mediated immunotherapy. Myeloid-derived suppressor cells (MDSC) represent an important constituent of this immunosuppressive milieu. Large numbers of MDSC are present in and near tumor sites where they inhibit the activity of Ag-specific T and NK cells. Current studies indicate that the delivery of CpG ODN directly into the tumor bed reduces the immunosuppressive activity of monocytic (CD11b(+), Ly6G(-), Ly6C(high)) MDSC. Monocytic MDSC express TLR9 and respond to CpG stimulation by 1) losing their ability to suppress T cell function, 2) producing Th1 cytokines, and 3) differentiating into macrophages with tumoricidal capability. These findings provide insight into a novel mechanism by which CpG ODN contribute to tumor regression, and they support intratumoral injection as the optimal route for their delivery. The Journal of Immunology, 2012, 188: 1592-1599.

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External Sources

  1. View Full Text
  2. DOI: 10.4049/jimmunol.1101304
  3. View record in Web of Science®
  4. WOS: 000300139000004

Library Notes

  1. Fiscal Year: FY2011-2012
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