OX40 enhances T cell immune response to PD-1 blockade therapy in non-small cell lung cancer

Int Immunopharmacol. 2022 Jul:108:108813. doi: 10.1016/j.intimp.2022.108813. Epub 2022 May 14.

Abstract

Immune-checkpoint blockade is widely studied for cancer therapy. Although the co-inhibitory receptor Programmed death-1(PD-1) blockade benefits some non-small cell lung cancer (NSCLC) patients, a large portion of NSCLC patients still fail to respond to this immunotherapy, and the underlying mechanism is unclear. Thus, a synergistic therapy to enhance the effect of PD-1 is urgently needed to improve the poor outcome of NSCLC patients. Here, we demonstrated that effector memory T cells were increased and T cell response became stronger in PD-1 immunotherapy responders (n = 20) but not in non-responders (n = 10). The expression of co-stimulatory receptor OX40 was upregulated on T cells following PD-1 immunotherapy and was positively associated with the percentage of PD-1+T cells and the responsiveness of T cells. Combination treatment of antagonistic anti-PD-1 and agonistic anti-OX40 antibodies (Abs) promoted the proliferation and cytokines production of T cells from PBMCs of non-responders ex vivo. Consistently, anti-PD-1 and anti-OX40 therapy synergistically augmented T cell response in an in vivo mouse lung cancer model. Our study confirmed the antitumor effects of anti-PD-1/OX40 combination in lung cancer patients as well as in the murine lung cancer model, and the results provide a rationale for clinical trials evaluating the therapeutic effect of this combination of antibodies for NSCLC immunotherapy.

Keywords: Combination immunotherapy; Immune checkpoint; NSCLC; OX40; PD-1.

MeSH terms

  • Animals
  • Antibodies / therapeutic use
  • B7-H1 Antigen
  • Carcinoma, Non-Small-Cell Lung* / drug therapy
  • Carcinoma, Non-Small-Cell Lung* / pathology
  • Humans
  • Immunity
  • Immunotherapy / methods
  • Lung Neoplasms* / drug therapy
  • Mice
  • Programmed Cell Death 1 Receptor

Substances

  • Antibodies
  • B7-H1 Antigen
  • Programmed Cell Death 1 Receptor