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Area of Science:

  • Immunology
  • Cancer Biology
  • Cellular Stress Response

Background:

  • The endoplasmic reticulum (ER) is crucial for immune cell function and antitumour immunity.
  • Tumor microenvironments induce ER stress, disrupting immune cell homeostasis and promoting cancer progression.
  • Dysregulated ER stress responses critically influence cancer immunity and immune escape.

Purpose of the Study:

  • To review how tumor-induced ER stress impacts immune cell function within the tumor microenvironment.
  • To highlight ER stress's role in limiting endogenous antitumour immunity and immunotherapy effectiveness.
  • To discuss therapeutic strategies targeting ER stress for enhanced cancer immunotherapy.

Main Methods:

  • Literature review of studies on ER stress, the unfolded protein response (UPR), and cancer immunity.
  • Analysis of mechanisms by which ER stress affects immune cells in the tumor microenvironment.
  • Synthesis of current research on UPR-targeted interventions in cancer immunotherapy.

Main Results:

  • Tumor-induced ER stress disrupts immune cell function, leading to chronic UPR activation.
  • ER stress curtails endogenous antitumour immune responses and diminishes immunotherapy efficacy.
  • Targeting ER stress pathways presents a viable therapeutic avenue for cancer treatment.

Conclusions:

  • ER stress is a key modulator of the tumor immune microenvironment and a significant barrier to effective cancer immunotherapy.
  • Restoring ER homeostasis and modulating UPR pathways can enhance antitumour immunity.
  • Targeting ER stress offers a novel approach to improve patient outcomes in cancer immunotherapy.