Intracellular mechanisms of tumor cells' immunoresistance

Acta Biochim Pol. 2020 Apr 22;67(2):143-148. doi: 10.18388/abp.2020_2878.

Abstract

One of the main mechanisms for avoiding immune response by cancer cells is mediated by inducing an immunosuppressive environment in the tumor following activation of immune checkpoints, i.e. PD-1 or CTLA-4 receptor inhibitors on T lymphocytes. Interaction inhibition between PD-1 or CTLA-4 and their ligands (PD-L1, CD80, and CD85) leads to unblocking of the T-lymphocyte function, and thus destroys cancer cells. Certain intracellular signaling pathways are also involved in the development of tumor cell immunoresistance. Immunosuppressive pathways' activation blocking may increase the immunological anti-tumor control.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • B7-H1 Antigen / antagonists & inhibitors
  • B7-H1 Antigen / metabolism*
  • CTLA-4 Antigen / antagonists & inhibitors
  • CTLA-4 Antigen / metabolism*
  • Female
  • Humans
  • Immune Tolerance
  • Lymphocyte Activation / drug effects
  • Male
  • Molecular Targeted Therapy / methods
  • Programmed Cell Death 1 Receptor / antagonists & inhibitors
  • Programmed Cell Death 1 Receptor / metabolism*
  • Signal Transduction / drug effects
  • T-Lymphocytes, Regulatory / immunology*
  • Tumor Escape*
  • Tumor Microenvironment / immunology*

Substances

  • Antineoplastic Agents
  • B7-H1 Antigen
  • CD274 protein, human
  • CTLA-4 Antigen
  • CTLA4 protein, human
  • PDCD1 protein, human
  • Programmed Cell Death 1 Receptor