A novel combination of chemotherapy and immunotherapy controls tumor growth in mice with a human immune system

Oncoimmunology. 2019 Apr 12;8(7):1596005. doi: 10.1080/2162402X.2019.1596005. eCollection 2019.

Abstract

Mice reconstituted with a human immune system and bearing human tumors represent a promising model for developing novel cancer immunotherapies. Here, we used mass cytometry and multi-parametric flow cytometry to characterize human leukocytes infiltrating a human breast cancer tumor model in immunocompromised NOD.SCID.γc-null mice reconstituted with a human immune system and compared it to samples of breast cancer patients. We observed highly activated human CD4+ and CD8+ T cells in the tumor, as well as minor subsets of innate immune cells in both settings. We also report that ICOS+ CD4+ regulatory T cells (Treg) were enriched in the tumor relative to the periphery in humanized mice and patients, providing a target to affect Treg and tumor growth. Indeed, administration of a neutralizing mAb to human ICOS reduced Treg proportions and numbers and improved CD4 + T cell proliferation in humanized mice. Moreover, a combination of the anti-ICOS mAb with cyclophosphamide reduced tumor growth, and that was associated with an improved CD8 to Treg ratio. Depletion of human CD8+ T cells or of murine myeloid cells marginally affected the effect of the combination therapy. Altogether, our results indicate that a combination of anti-ICOS mAb and chemotherapy controls tumor growth in humanized mice, opening new perspectives for the treatment of breast cancer. One sentence summary: Targeting ICOS in combination with chemotherapy is a promising strategy to improve tumor immunity in humans.

Keywords: ICOS; chemotherapy; cyclophosphamide; humanized mice; immunotherapy; regulatory T cells.

Publication types

  • Research Support, Non-U.S. Gov't

Grants and funding

This study was supported by the Ligue Nationale contre le cancer (LNC), the Agence Nationale de la Recherche (ANR-11-EMMA-0045 VICIT) and Glaxo Smith Kline (GSK). Dr A. Burlion was supported by a doctoral fellowship from the French Ministère de l’Education Supérieure et de la Recherche and from LNC. Dr K. Sendeyo was supported by a research contract with GSK. Pukar KC is supported by a doctorate fellowship from the Institut Universitaire de Cancérologie (Sorbonne Université).