Influence of lactate in resistance to anti‑PD‑1/PD‑L1 therapy: Mechanisms and clinical applications (Review)

Mol Med Rep. 2025 Feb;31(2):48. doi: 10.3892/mmr.2024.13413. Epub 2024 Dec 13.

Abstract

Metabolic reprogramming is a prominent characteristic of tumor cells, evidenced by heightened secretion of lactate, which is linked to tumor progression. Furthermore, the accumulation of lactate in the tumor microenvironment (TME) influences immune cell activity, including the activity of macrophages, dendritic cells and T cells, fostering an immunosuppressive milieu. Anti‑programmed cell death protein 1 (PD‑1)/programmed death‑ligand 1 (PD‑L1) therapy is associated with a prolonged survival time of patients with non‑small cell lung cancer. However, some patients still develop resistance to anti‑PD‑1/PD‑L1 therapy. Lactate is associated with resistance to anti‑PD‑1/PD‑L1 therapy. The present review summarizes what is known about lactate metabolism in tumor cells and how it affects immune cell function. In addition, the present review emphasizes the relationship between lactate secretion and immunotherapy resistance. The present review also explores the potential for targeting lactate within the TME to enhance the efficacy of immunotherapy.

Keywords: cancer immunity; immunotherapy; lactate; programmed cell death protein 1; programmed death‑ligand 1; tumor environment.

Publication types

  • Review

MeSH terms

  • Animals
  • B7-H1 Antigen* / metabolism
  • Carcinoma, Non-Small-Cell Lung / drug therapy
  • Carcinoma, Non-Small-Cell Lung / immunology
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / pathology
  • Drug Resistance, Neoplasm*
  • Humans
  • Immune Checkpoint Inhibitors / pharmacology
  • Immune Checkpoint Inhibitors / therapeutic use
  • Immunotherapy / methods
  • Lactic Acid* / metabolism
  • Neoplasms / drug therapy
  • Neoplasms / immunology
  • Neoplasms / metabolism
  • Programmed Cell Death 1 Receptor / antagonists & inhibitors
  • Programmed Cell Death 1 Receptor / metabolism
  • Tumor Microenvironment* / immunology

Substances

  • Lactic Acid
  • B7-H1 Antigen
  • Immune Checkpoint Inhibitors
  • Programmed Cell Death 1 Receptor
  • CD274 protein, human
  • PDCD1 protein, human

Grants and funding

The present study was supported by the National Natural Science Foundation of China (grant nos. 82103004 and 82273323).