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Related Experiment Video

Updated: Mar 25, 2026

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RETREG1-Mediated Reticulophagy is Essential for Dendritic Cell Maturation and Function in Sepsis.

Ren-Qi Yao1,2, Chao Ren2,3, Li-Yu Zheng2

  • 1Department of General Surgery, The First Medical Center of Chinese PLA General Hospital, Beijing, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|March 24, 2026
PubMed
Summary
This summary is machine-generated.

Reticulophagy regulator 1 (RETREG1) is vital for dendritic cell (DC) function during sepsis. RETREG1 maintains DC maturation and antigen presentation by reducing endoplasmic reticulum stress, crucial for combating lethal infections.

Keywords:
autophagydendritic cellsendoplasmic reticulumimmunosuppressionreticulophagysepsis

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Dendritic cells (DCs) are critical for immune responses during infections.
  • Sepsis involves complex immune dysregulation impacting DC function.
  • Endoplasmic reticulum (ER) stress is implicated in sepsis pathogenesis.

Purpose of the Study:

  • To investigate the role of reticulophagy regulator 1 (RETREG1) in dendritic cell function during early sepsis.
  • To elucidate the molecular mechanisms by which RETREG1 influences DC maturation and antigen presentation under ER stress.

Main Methods:

  • Utilized mouse models with genetic deletions in Retreg1 and Atf6.
  • Investigated RETREG1 expression and function in response to lipopolysaccharide (LPS).
  • Analyzed ER stress, autophagy pathways (EIF2AK3), and MHC-II ubiquitination (MARCH8) in DCs.
  • Performed single-cell bioinformatics analysis on human septic patient samples.

Main Results:

  • RETREG1 maintains DC maturation and function in early sepsis.
  • Activating transcription factor 6 (ATF6) directly regulates RETREG1 expression under LPS-induced ER stress.
  • RETREG1-mediated reticulophagy alleviates ER stress via EIF2AK3 signaling.
  • RETREG1 prevents MARCH8-dependent MHC-II ubiquitination, preserving antigen presentation.
  • Mice lacking RETREG1 or ATF6 show impaired DC function, leading to immunosuppression and organ failure in sepsis.
  • Deficits in DC reticulophagy correlate with human sepsis development.

Conclusions:

  • RETREG1 is a key mediator of DC function and immune homeostasis during sepsis.
  • Targeting RETREG1-mediated reticulophagy may offer therapeutic strategies for sepsis.
  • DC reticulophagy represents a potential biomarker and therapeutic target in human sepsis.