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A One-Two Punch By The Immune System Knocks Out Cancer Cells

An emerging class of therapies called “checkpoint blockade” enhance ’s ability to attack cancer cells by interfering with the immunological checkpoints that slow or stop immune cell activation and proliferation in the presence of tumors. Cytotoxic T lymophocyte antigen-A (CTLA) receptor is a that acts like an “off switch” on certain . Antibodies targeting CTLA can keep the protein from turning the off and allow them to attach tumor cells.

In this issue of the Journal of Clinical Investigation, Sandra Demaria and her colleagues at identified factors that determine the effectiveness of anti-CTLA therapy by tracking the activity of immune cells in a mouse model of . In this model anti-CTLA therapy alone was ineffective. When given in combination with radiation treatment, however, tumor growth and mestastases was significantly reduced. The researchers found that the caused the cancer cells to release a protein, NKG2D, which activates the immune cells and attracts them to the tumor. These findings will be critical in developing improved treatment regimens utilizing CTLA antibodies.


“Suppressing T cell motility induced by anti–CTLA-4 monotherapy improves antitumor effects” Sandra Demaria, New York University School of Medicine, New York, NY, USA

Journal of Clinical Investigation Sept. 4, 2012