Engineered immune cells aimed at CD28 reduced leukemia growth in cultures and mice carrying human cancer. This single peer-reviewed study identified a potential target using childhood leukemia samples, then tested cell designs against it. Some healthy helper cells were also depleted, and one cancer model escaped as the target diminished. Clinical benefit remains untested.
Immune cells engineered to recognize CD28 suppressed leukemia in cell cultures and in mice carrying human leukemia. The single peer-reviewed study published on 8 October tests a laboratory approach rather than a treatment given to patients. CD28 is a surface molecule present on cancer cells and some healthy immune cells; selecting it as a target therefore involves both cancer recognition and effects on the wider immune system.[1]
The target search compared marrow from 14 healthy donors with samples from 54 childhood cases of acute lymphoblastic leukemia of T-cell origin. A screen of 25 surface targets detected CD28 in 81.5% of leukemia cases. The team tested 20 receptor designs, found five functional versions and selected two for further work. Gene editing removed CD28 from the treatment cells themselves to prevent mutual attack during their production.[1]
In the mouse experiments, disease grew more slowly and survival increased. Activity resembled that of cells aimed at CD7, the laboratory benchmark. In healthy-cell cocultures, the CD28 approach left a larger share of CD8 T cells and natural killer cells intact, but depleted CD4 helper cells. One leukemia model escaped while CD28 expression fell. These results leave patient safety, target loss and the range of responsive cancers for clinical investigation.[1]
