Anti-LAG-3 boosts CD8 T cell effector function

Courtney T Kureshi; Michael Dougan; Stephanie K Dougan

doi:10.1016/j.cell.2024.07.004

Anti-LAG-3 boosts CD8 T cell effector function

Cell. 2024 Aug 8;187(16):4144-4146. doi: 10.1016/j.cell.2024.07.004.

Authors

Courtney T Kureshi¹, Michael Dougan², Stephanie K Dougan³

Affiliations

¹ Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA; Program in Immunology, Harvard Medical School, Boston, MA, USA.
² Program in Immunology, Harvard Medical School, Boston, MA, USA; Division of Gastroenterology, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.
³ Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA; Program in Immunology, Harvard Medical School, Boston, MA, USA. Electronic address: stephanie_dougan@dfci.harvard.edu.

PMID: 39121844
DOI: 10.1016/j.cell.2024.07.004

Abstract

LAG-3 is the third immune checkpoint pathway successfully targeted for cancer therapy. Although ineffective as a monotherapy, combination of LAG-3 and PD-1 blockade improves survival from advanced melanoma. In this issue of Cell, two studies in mice and a human clinical trial provide insights on LAG-3 in immune regulation.

Publication types

Comment

MeSH terms

Animals
Antigens, CD* / immunology
Antigens, CD* / metabolism
CD8-Positive T-Lymphocytes* / immunology
Humans
Immune Checkpoint Inhibitors / pharmacology
Immune Checkpoint Inhibitors / therapeutic use
Lymphocyte Activation Gene 3 Protein*
Melanoma / drug therapy
Melanoma / immunology
Mice
Programmed Cell Death 1 Receptor / antagonists & inhibitors
Programmed Cell Death 1 Receptor / immunology
Programmed Cell Death 1 Receptor / metabolism

Substances

Lymphocyte Activation Gene 3 Protein
Antigens, CD
Programmed Cell Death 1 Receptor
Immune Checkpoint Inhibitors