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Inhibition of the B7-H3 immune checkpoint limits tumor growth by enhancing cytotoxic lymphocyte function

Young-Hee Lee1, Natalia Martin-Orozco1,2, Peilin Zheng3,4,5

  • 1Department of Immunology.

Cell Research
|July 8, 2017
PubMed

Insights

The B7-H3 checkpoint inhibits anti-tumor immunity. Blocking B7-H3 enhances immune responses against cancer, offering a new target for immunotherapy.

Area of Science:

  • Immunology
  • Oncology
  • Cancer Research

Background:

  • Tumor-immune system interactions are complex and not fully understood.
  • Current immunotherapies targeting CTLA4 and PD-1/PD-L1 show limited response rates.
  • Additional co-inhibitory molecules are needed for effective cancer treatment.

Purpose of the Study:

  • To investigate the role of B7-H3 in tumor immunity.
  • To evaluate B7-H3 as a potential target for cancer immunotherapy.

Main Methods:

  • Analysis of B7-H3 expression in tumor cells and immune cells.
  • Utilizing B7-H3-deficient mice and antagonistic antibodies.
  • Assessing the impact of B7-H3 blockade on tumor growth and immune cell function.
  • Combination therapy with B7-H3 and PD-1 blockade.

Main Results:

  • B7-H3 is expressed in various tumor types and tumor-infiltrating immune cells.
  • B7-H3 deficiency or blockade reduces tumor growth, dependent on NK and CD8+ T cells.
  • B7-H3 inhibits cytotoxic lymphocyte activation; its blockade enhances their function.
  • Combined blockade of B7-H3 and PD-1 improves therapeutic control of advanced tumors.

Conclusions:

  • B7-H3 acts as a co-inhibitory checkpoint in tumor immunity.
  • Targeting B7-H3 represents a promising novel strategy for cancer immunotherapy.
  • Combination therapies involving B7-H3 blockade may overcome resistance to existing treatments.

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