Endoplasmic reticulum stress and unfolded protein response in immune cell function

Area of Science:

• Immunology
• Cellular Biology
• Molecular Biology

Background:

• Endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) are key regulators of immune cell function and inflammation.
• The UPR, involving sensors IRE1α, PERK, and ATF6, maintains homeostasis but can drive disease when dysregulated.
• Emerging evidence highlights UPR's roles in immune cell fate, activation, and cytokine production.

Purpose of the Study:

• To provide a comprehensive overview of ER stress and UPR influence on various immune cell types.
• To explore the cell-type-specific and context-dependent functions of ER stress responses in immunity.
• To underscore the importance of understanding these mechanisms for targeted therapeutic development.

Main Methods:

• Literature review synthesizing recent findings on ER stress and UPR in immunology.
• Analysis of studies investigating UPR's impact on immune cell subsets.
• Integration of knowledge on peripheral and central immune system components.

Main Results:

• ER stress and UPR significantly influence immune cell function, fate, and inflammatory responses.
• Dysregulation of UPR contributes to immune-related pathogenesis.
• Specific roles of ER stress vary across different immune cell types, including monocytes, macrophages, dendritic cells, granulocytes, T cells, B cells, microglia, and astrocytes.

Conclusions:

• Understanding the intricate roles of ER stress and UPR in diverse immune cells is critical.
• Targeted therapies modulating ER stress pathways hold potential for treating inflammatory and immune-related diseases.
• Further research is needed to fully elucidate context-dependent UPR functions in specific immune cell populations.