The success of a cancer therapy that unleashes immune cells on tumours depends on the cells producing a protein called CD28. The molecule could serve as a biomarker for selecting individuals who are likely to respond to certain immunotherapies.
Drugs that inhibit a protein called PD-1 can boost the proliferation of immune cells called T cells and their anti-cancer activity, but the strategy works in only a fraction of patients. Rafi Ahmed at Emory University in Atlanta, Georgia, and his colleagues found that when they chemically blocked the activity of CD28, which is made by T cells, tumours kept growing in mice, even when the animals were treated with anti-PD-1 drugs. In patients with lung cancer whose T cells proliferated after receiving PD-1 therapy, those cells tended to express CD28.
In a separate study, Ronald Vale at the University of California, San Francisco, Ira Mellman at Genentech in South San Francisco and their colleagues found that PD-1 and CD28 are part of the same biochemical pathway. They report that PD-1 signalling suppresses T-cell function by inactivating CD28 activity.
Science http://doi.org/b2vs; http://doi.org/b2vt (2017)
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Drug success factor found. Nature 543, 290 (2017). https://doi.org/10.1038/543290c
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DOI: https://doi.org/10.1038/543290c