Interferon Biology and LAG-3 Shedding in PD-(L)1 plus LAG-3 Immunotherapy

Clin Cancer Res. 2023 Mar 1;29(5):835-837. doi: 10.1158/1078-0432.CCR-22-3312.

Abstract

Targeting coinhibitory receptors on dysfunctional T cells may improve response to anti-PD-(L)1 in the IFNγ associated T-cell-inflamed tumor microenvironment. The bispecific lymphocyte activation gene 3 (LAG-3) and PD-L1 blocking antibody FS118, potentially through LAG-3 shedding, represents a promising strategy to improve immune checkpoint blockade. Soluble LAG-3 is an intriguing biomarker for LAG-3 drug activity. See related article by Yap et al., p. 888.

Publication types

  • Editorial
  • Research Support, N.I.H., Extramural
  • Comment

MeSH terms

  • Antibodies, Bispecific* / pharmacology
  • Antineoplastic Agents* / pharmacology
  • B7-H1 Antigen
  • Biology
  • Humans
  • Immunotherapy
  • Interferons
  • Neoplasms* / drug therapy
  • Neoplasms* / genetics
  • Tumor Microenvironment / drug effects

Substances

  • Interferons
  • B7-H1 Antigen
  • Antineoplastic Agents
  • Antibodies, Bispecific