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Targeting TNFR2, an immune checkpoint stimulator and oncoprotein, is a promising treatment for cancer

Xin Chen1,2, Joost J Oppenheim3

  • 1State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao S.A.R. 999078, China. xchen@umac.mo oppenhej@mail.nih.gov.

Science Signaling
|January 19, 2017
PubMed

Insights

Dominant antagonistic antibodies targeting tumor necrosis factor receptor 2 (TNFR2) show promise for ovarian cancer. This therapy may suppress regulatory T cells (Tregs) and induce cancer cell death, potentially enhancing antitumor immunity.

Area of Science:

  • Immunology
  • Oncology
  • Cancer Biology

Background:

  • Tumor necrosis factor receptor 2 (TNFR2) is present on cancer cells and tumor-infiltrating immunosuppressive CD4+FoxP3+ regulatory T cells (Tregs).
  • TNFR2 signaling promotes Treg activation, proliferation, and immune suppression, contributing to cancer cell survival and tumor growth.
  • Tregs represent a significant barrier to effective antitumor immune responses.

Purpose of the Study:

  • To investigate the therapeutic potential of targeting TNFR2 in ovarian cancer.
  • To evaluate the dual action of TNFR2 antagonism on both Tregs and cancer cells.

Main Methods:

  • Development and application of dominant antagonistic antibodies against human TNFR2.
  • Assessment of antibody effects on Treg activity and proliferation.
  • Evaluation of antibody-induced cancer cell death.

Main Results:

  • Antagonistic antibodies against TNFR2 effectively suppressed Treg activation and proliferation.
  • These antibodies also induced death in cancer cells.
  • The dual action suggests a novel therapeutic strategy.

Conclusions:

  • Dominant antagonistic TNFR2 antibodies represent a potential therapeutic strategy for ovarian cancer.
  • This approach simultaneously targets immunosuppressive Tregs and promotes cancer cell apoptosis.
  • Further research is warranted to explore clinical applications.

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