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Clinical blockade of PD1 and LAG3--potential mechanisms of action

Linh T Nguyen1, Pamela S Ohashi1

  • 1Immune Therapy Program, Princess Margaret Cancer Centre, 610 University Avenue, Toronto, Ontario, M5G 2M9, Canada.

Nature Reviews. Immunology
|December 24, 2014
PubMed

Insights

Dysfunctional T cells hinder immune responses against infections and cancer. This review explores how targeting inhibitory receptors like programmed cell death protein 1 (PD1) and lymphocyte activation gene 3 protein (LAG3) can restore T cell function.

Area of Science:

  • Immunology and Cancer Biology
  • T cell immunology
  • Immune checkpoint inhibition

Background:

  • T cell dysfunction impairs the immune system's ability to fight infections and cancer.
  • Therapeutic strategies targeting inhibitory T cell surface receptors show promise in clinical settings.
  • Understanding these inhibitory pathways is crucial for effective cancer immunotherapy.

Purpose of the Study:

  • To review the mechanisms of action for agents targeting PD1 and LAG3.
  • To discuss the role of these targets in T cell inhibition.
  • To propose correlative studies for mechanism elucidation and biomarker identification.

Main Methods:

  • Literature review of clinical agents targeting PD1 and LAG3.
  • Analysis of potential mechanisms of T cell inhibition by PD1 and LAG3.
  • Discussion of correlative studies and biomarker development.

Main Results:

  • PD1 and LAG3 are key inhibitory receptors on T cells.
  • Clinical agents targeting PD1 and LAG3 aim to restore T cell anti-tumor activity.
  • Further research is needed to define precise mechanisms and identify predictive biomarkers.

Conclusions:

  • Targeting PD1 and LAG3 represents a significant advance in cancer immunotherapy.
  • Elucidating the mechanisms of action will optimize therapeutic strategies.
  • Identifying biomarkers will improve patient selection and treatment efficacy.

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