Tumors (purple cells) recruit abnormally high numbers of potently immune-suppressing Tregs, which repress effector T cells (1) and prevent cancer destruction. Addition of anti-TNFR2 monoclonal antibodies (2) targets and kills TNFR2-expressing Tregs, thereby boosting the activity of effector T cells, which attack the tumor (3). The antibodies can also directly kill tumor cells that express the TNFR2 receptor.© GEORGE RETSECK
Tumors are adept at locally suppressing the body’s immune system, creating a microenvironment that allows unchallenged survival and growth. One way they do this is by recruiting high numbers of regulatory T cells, a type of naturally immunosuppressive T cells known as Tregs or Tregs.
To counter this suppression, scientists are investigating ways to boost cancer patients’ immune systems to encourage tumor destruction. But it’s a delicate balance: too much immune activation and there’s a risk of potentially lethal autoimmune disorders—as has been reported for some patients treated with the immune system–activating drugs ipilimumab (Yervoy) and nivolumab (Opdivo).
Searching for a more refined approach to immunotherapy, Denise Faustman and colleagues at Massachusetts General Hospital and Harvard Medical School have discovered that many tumors recruit a ...
