Weill Cornell researchers have found a way to wake up exhausted T cells and boost cancer-fighting power, according to the Cornell Chronicle.
The study revealed tumors hijack a protein called CD47 on T cells, using it—alongside a partner molecule, thrombospondin-1—to switch off the immune response. Blocking this interaction in mice revived T cell activity and slowed tumor growth.
A peptide called TAX2 disrupted the CD47 signal and worked even better when combined with existing immunotherapy, paving the way for stronger, longer-lasting cancer treatments.
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