“We expected to find exhausted T cells with epigenomes damaged beyond repair,” Pholek recalled.
But, they discovered the opposite. Pholek and her team found that gene expression could be increased using an antibody known as 4-1BB, which subsequently enhanced T cell activity.
Another crucial finding was that low oxygen levels, also known as hypoxia, significantly contribute to decreased gene expression among exhausted T cells.
“By restoring oxygen or improving co-stimulation, we can realize the full potential of these cells and potentially gain the benefits of a functioning, healthy immune system,” said Greg Delgoffe, the study’s co-senior author.
Now, the researchers are hopeful these findings could inform new approaches to targeting T cell terminal exhaustion– including immunotherapy drugs that specifically target hypoxia, co-stimulation, or engineer exhaustion-resistant T cells known as CAR-T.
To read the study’s complete findings, visit the link here.
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